Affinage

CXCL1

Growth-regulated alpha protein · UniProt P09341

Length
107 aa
Mass
11.3 kDa
Annotated
2026-06-09
100 papers in source corpus 40 papers cited in narrative 40 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CXCL1 (GROα/MGSA) is a secreted ELR-containing CXC chemokine that drives neutrophil recruitment, angiogenesis, and oncogenic transformation by signaling through CXCR2 (PMID:2271650, PMID:8380167, PMID:11030154). The mature protein is a non-glycosylated ~71-residue polypeptide that competes with IL-8 for neutrophil receptors and is chemotactic for neutrophils (PMID:2271650), while also engaging a CXCL1-specific high-affinity receptor on melanoma cells to drive proliferation (PMID:8380167). Receptor engagement requires an intact ELR motif and triggers CXCR2-dependent outputs that bifurcate downstream: a cdc42–PAK1 cascade mediates chemotaxis independently of ERK, separable from CXCR2-evoked Ca2+ mobilization (PMID:12033944), and a PKCμ–ILK pathway couples CXCR2 to NLRP3 inflammasome activation and IL-1β production (PMID:28739876). CXCL1 exists as monomers and disulfide-trapped dimers that are both active CXCR2 agonists engaging the receptor N-terminus, with the dimer serving as the high-affinity glycosaminoglycan ligand through two structurally distinct, non-overlapping GAG-binding domains (α and β), and in vivo neutrophil recruitment requires both receptor activation and GAG binding acting synergistically (PMID:23479735, PMID:26721883, PMID:27625115, PMID:32881070). Transcription of CXCL1 is governed by an enhanceosome-like assembly of NF-κB, Sp1/Sp3, and HMGI(Y) at the proximal promoter (PMID:7479086), and constitutive overexpression in melanoma arises from elevated IKK activity driving IκBα degradation and nuclear NF-κB localization (PMID:10096573); cytokine induction additionally operates through mRNA stabilization, STAT1 recruitment, and histone H3 modification (PMID:8264646, PMID:24280128). Through CXCR2, CXCL1 induces neutrophil and MDSC trafficking that produces immunosuppressive, T-cell-excluding tumor microenvironments sustained by feed-forward neutrophil-derived TNF–TNFR2 circuits (PMID:35700773, PMID:36946782), promotes angiogenesis via VEGF-A (PMID:33770315), and activates Ras/AP-1 to transform melanocytes (PMID:11030154). CXCL1/CXCR2 signaling is a recurrent driver of neutrophil-mediated pathology across infection, vaso-occlusive crisis, encephalitis, and neuropathic pain (PMID:28739876, PMID:21383500, PMID:32937134, PMID:30991054).

Mechanistic history

Synthesis pass · year-by-year structured walk · 27 steps
  1. 1989 Medium

    Established that CXCL1 is an inducible endothelial chemokine, defining the upstream inflammatory signals (IL-1, TNF, LPS, thrombin) and an autocrine amplification loop that drive its expression.

    Evidence Northern blot, ELISA, TPA/PKC pharmacology, and recombinant cytokine stimulation of primary HUVEC cultures

    PMID:2670560

    Open questions at the time
    • Did not resolve the promoter elements or transcription factors mediating induction
    • PKC involvement inferred pharmacologically from TPA only
  2. 1990 High

    Defined CXCL1 as a mature non-glycosylated chemokine that competes with IL-8 for neutrophil receptors and is melanoma-mitogenic, linking a single ligand to both chemotactic and growth-promoting activities.

    Evidence Recombinant expression, mass spectrometry, N-terminal sequencing, receptor competition binding, and neutrophil chemotaxis assays; separate melanocyte/melanoma proliferation assays

    PMID:2095366 PMID:2271650

    Open questions at the time
    • Receptor mediating mitogenic activity not yet molecularly identified
    • Mechanism connecting receptor binding to proliferation undefined
  3. 1991 High

    Demonstrated that CXCL1 is not merely a marker but a causal oncogenic driver, as forced expression confers anchorage independence and tumorigenicity.

    Evidence Stable transfection of melan-a melanocytes, soft-agar colony assays, nude mouse xenografts, and ploidy analysis

    PMID:1861861

    Open questions at the time
    • Did not identify the receptor or downstream signaling required for transformation
    • Source of aneuploidy unexplained
  4. 1993 High

    Resolved receptor usage by distinguishing a CXCL1-specific high-affinity receptor on melanoma from the shared CXCR2 used in monocytic cells, connecting ligand binding to proliferation and Ca2+ signaling.

    Evidence 125I-MGSA radioligand binding with Scatchard analysis, cross-competition with IL-8, and Ca2+ flux cross-desensitization assays

    PMID:8380167

    Open questions at the time
    • Molecular identity of the melanoma-specific receptor not established
    • Signaling between receptor and proliferation not mapped
  5. 1994 High

    Separated transcriptional from post-transcriptional control, showing melanoma elevates basal transcription while cytokines act largely via mRNA stabilization, and pinpointed NF-κB as the cytokine-responsive promoter element.

    Evidence Nuclear run-off, CAT reporter with promoter deletion/mutation, EMSA, and mRNA half-life measurements

    PMID:8264646

    Open questions at the time
    • Did not identify the full enhanceosome composition
    • Upstream cause of elevated basal transcription in melanoma unresolved
  6. 1995 High

    Defined the composite promoter architecture, establishing that NF-κB, Sp1/Sp3, and HMGI(Y) cooperate as an enhanceosome-like complex required for both basal and induced transcription.

    Evidence CAT reporter assays with deletion/point mutations, EMSA, and DNase I footprinting

    PMID:7479086

    Open questions at the time
    • Did not determine the signaling driving constitutive NF-κB activity
    • Functional cooperativity among factors inferred from mutagenesis
  7. 1997 High

    Linked CXCL1-driven tumorigenesis to paracrine angiogenesis and constitutive NF-κB, and extended its growth-promoting role to keratinocytes and wound healing.

    Evidence SCID/nude xenografts with anti-CXCL1 neutralization, conditioned-medium angiogenesis assays, and keratinocyte proliferation plus in vivo wound-healing models

    PMID:9143736 PMID:9365113

    Open questions at the time
    • Molecular angiogenic effectors not identified
    • Shortened IκB half-life mechanism not yet causally tested
  8. 1999 High

    Identified constitutively elevated IKK activity as the cause of nuclear NF-κB and elevated CXCL1 in melanoma, providing the causal upstream lesion.

    Evidence IKK immunoprecipitation-kinase assays, phospho-IκBα detection, proteasome inhibition, and dominant-negative IKKα/IκBα reporter rescue

    PMID:10096573

    Open questions at the time
    • Did not identify what activates IKK in melanoma
    • Connection to downstream transformation phenotype not directly tested here
  9. 2000 High

    Placed Ras/AP-1 downstream of CXCL1 in transformation and showed transformation requires the ELR motif and CXCR2 affinity, unifying the autocrine growth and paracrine angiogenic mechanisms.

    Evidence Differential display, AP-1 reporter assays, dominant-negative and constitutively active M-Ras, ELR-mutant CXCL1, and soft-agar plus athymic-mouse xenografts with antiserum neutralization

    PMID:10647998 PMID:11030154

    Open questions at the time
    • Intermediate signaling between CXCR2 and Ras activation not defined
    • How M-Ras induction is achieved transcriptionally unresolved
  10. 2002 High

    Dissected CXCR2 downstream signaling, showing chemotaxis requires a cdc42–PAK1 cascade acting independently of ERK and separable from Ca2+ mobilization.

    Evidence Dominant-negative constructs, kinase activity assays, MEK inhibitor pharmacology, and Boyden-chamber chemotaxis plus Ca2+ assays in CXCR2-expressing HEK293 cells

    PMID:12033944

    Open questions at the time
    • Did not connect cdc42-PAK1 to in vivo recruitment
    • G-protein coupling upstream of cdc42 not defined
  11. 2005 Medium

    Connected matrix-derived hyaluronan signaling to CXCL1, identifying CD44-dependent CXCL1 induction as a required step in angiogenic morphogenesis.

    Evidence Microarray, CD44-blocking and anti-CXCL1 neutralization in 3D collagen tube-formation assays

    PMID:15843382

    Open questions at the time
    • Signaling between CD44 and CXCL1 transcription not mapped
    • In vivo relevance not tested
  12. 2013 High

    Established the CXCL1 dimer as a fully active CXCR2 agonist engaging the receptor N-terminus, distinguishing it from inactive dimers of related chemokines.

    Evidence Disulfide-trapped dimer construction with CXCR2 binding, Ca2+ flux, internalization assays, and NMR characterization of the N-terminal interaction

    PMID:23479735

    Open questions at the time
    • In vivo significance of the dimer not yet tested
    • GAG-binding role of dimer not yet characterized in this study
  13. 2013 High

    Showed cytokine-induced CXCL1 transcription integrates NF-κB occupancy with STAT1 recruitment and histone H3 modification, expanding the regulatory mechanism beyond NF-κB alone.

    Evidence Promoter mutation, ChIP for p65/p50/STAT1/RNA Pol II, histone H3 modification analysis, and flow cytometry of neutrophil integrins in pancreatic β-cells

    PMID:24280128

    Open questions at the time
    • Kinase driving STAT1 serine phosphorylation not identified here
    • Histone modifier enzymes not defined
  14. 2015 High

    Defined the structural basis of glycosaminoglycan binding, identifying two non-overlapping GAG domains and showing GAG and receptor-binding surfaces overlap so GAG-bound CXCL1 occludes CXCR2.

    Evidence NMR chemical-shift mapping with heparin oligosaccharides, site-directed mutagenesis, and GAG-binding assays

    PMID:26721883

    Open questions at the time
    • Functional consequence of dual GAG domains in vivo not yet tested
    • How GAG and receptor binding are temporally coordinated unresolved
  15. 2016 High

    Demonstrated that in vivo neutrophil recruitment requires both CXCR2 activation and GAG binding acting synergistically, with the wild-type form outperforming locked monomers or dimers.

    Evidence Mutagenesis of α/β GAG domains, heparin affinity assays, and mouse peritoneal neutrophil recruitment with trapped monomer/dimer variants

    PMID:27625115

    Open questions at the time
    • Precise spatial gradient mechanism not directly visualized
    • Relative contribution of each domain across tissues unresolved
  16. 2016 High

    Linked CXCL1/CXCR2 to inflammasome biology by mapping a PKCμ–ILK pathway driving NLRP3 activation and IL-1β production during infection.

    Evidence siRNA knockdown, pharmacologic inhibition, NLRP3 activation assays, and carrageenan and M. tuberculosis in vivo models

    PMID:28739876

    Open questions at the time
    • How CXCR2 couples to PKCμ not defined
    • Cell-type specificity of the pathway beyond macrophages untested
  17. 2016 Medium

    Identified a non-canonical TLR2–IRAK–MST1/2–IRF3 Hippo axis as an upstream driver of CXCL1 secretion in macrophages during infection, broadening its inducing pathways.

    Evidence siRNA knockdown of MST1/2, TLR2/IRAK inhibition, ELISA, and paracrine co-culture in M. tuberculosis infection

    PMID:27883091

    Open questions at the time
    • Direct binding of IRF3 to CXCL1 promoter not demonstrated
    • Single-lab pathway placement
  18. 2018 High

    Resolved the spatiotemporal division of labor in neutrophil extravasation, showing endothelial/pericyte CXCL1 supports crawling while neutrophil CXCL2 mediates junction breaching.

    Evidence Intravital confocal microscopy in mouse cremaster muscle with CXCL1/CXCL2 and ACKR1 knockouts and cell-specific reporters

    PMID:30446388

    Open questions at the time
    • Receptor-level mechanism distinguishing the two chemokines not fully resolved
    • Generalizability across vascular beds untested
  19. 2019 High

    Connected mechanotransduction to CXCL1, defining an integrin–Notch1–Piezo axis that drives endothelial CXCL1 and neutrophil-mediated portal hypertension.

    Evidence Mechanical stretch device, RNA-seq, conditional Notch1 endothelial knockout, intravital imaging, and NE-/-/Pad4-/- mice with portal pressure measurement

    PMID:30872106

    Open questions at the time
    • Direct transcriptional link from Notch1 to CXCL1 promoter not shown
    • Role of Piezo Ca2+ signaling in transcription not isolated
  20. 2019 High

    Established CXCL1/CXCR2 as a sufficient driver of vaso-occlusive crisis in sickle cell disease, where recombinant CXCL1 alone induces acute VOC.

    Evidence Humanized SCD mouse model, recombinant CXCL1 administration, CXCR2 blockade, and intravital microscopy

    PMID:21383500

    Open questions at the time
    • Cellular source of pathogenic CXCL1 not defined
    • Downstream adhesion mechanism not detailed
  21. 2019 Medium

    Extended CXCL1/CXCR2 into multiple CNS and neuropathic pain settings, defining glial/neuronal sources and CXCR2-dependent neutrophil recruitment driving pathology.

    Evidence Intrathecal neutralization/antagonism, PI3Kγ and NF-κB inhibition, TLR4 and CXCL1 gene silencing, primary DRG cultures, and behavioral pain models across bone cancer pain, paclitaxel neuropathy, and EAE

    PMID:30606213 PMID:30991054 PMID:31427756

    Open questions at the time
    • Direct demonstration of neuron-targeted CXCR2 signaling varies by model
    • Single-lab pharmacologic dissection in each context
  22. 2020 High

    Defined CXCL1 as the critical CXCR2 ligand for neutrophil transendothelial migration and blood-brain barrier permeability in viral encephalitis, separating immunopathology from viral control.

    Evidence Cxcr2 knockout mice, HSV-1 encephalitis, intravital imaging, BBB permeability and viral titer measurements with cell-type-specific cytokine analysis

    PMID:32937134

    Open questions at the time
    • Mechanism of BBB disruption downstream of neutrophils not detailed
    • Relative roles of astrocyte vs neuron sources not quantified
  23. 2020 High

    Showed that monomer-dimer equilibrium and differential GAG/receptor activities of Cxcl1 versus Cxcl2 jointly tune neutrophil recruitment in a dose- and time-dependent manner.

    Evidence CXCR2 G-protein and β-arrestin assays, heparan sulfate binding, and mouse peritoneal recruitment with trapped dimer variants

    PMID:32881070

    Open questions at the time
    • Predictive model linking biophysical parameters to recruitment incomplete
    • In vivo monomer-dimer ratios not directly measured
  24. 2023 High

    Demonstrated that a Cxcl1-Cxcl2 heterodimer combines high GAG affinity with dampened receptor activity to maximize neutrophil recruitment, refining the structure-function logic of recruitment.

    Evidence Engineered heterodimer with CXCR2 activity assays, heparan sulfate binding, and in vivo peritoneal recruitment

    PMID:37625009

    Open questions at the time
    • Endogenous heterodimer formation in vivo not directly confirmed
    • Structural basis of dampened receptor activity not solved
  25. 2023 High

    Defined cell-autonomous CXCL1 as a driver of spatial T-cell exclusion in pancreatic cancer through CXCR2+ neutrophilic MDSCs, sustained by a neutrophil TNF–TNFR2 feed-forward circuit.

    Evidence Imaging mass cytometry, shRNA silencing of Cxcl1 in KPC cells, KPC mouse model, TNFR2 inhibition, bone marrow transplant, and co-culture

    PMID:36946782

    Open questions at the time
    • Transcriptional mechanism linking TNFR2 to CXCL1 reinduction not detailed
    • Human therapeutic translation untested
  26. 2024 Medium

    Linked tumor metabolism, transcription, and microenvironment by showing acetyl-CoA-driven H3 acetylation upregulates CXCL1 to recruit neutrophils and promote NET-dependent metastasis.

    Evidence Cytokine microarray, H3 acetylation ChIP at CXCL1, knockdown, CXCR2 inhibition, NET assays, and orthotopic HCC xenografts

    PMID:38670307

    Open questions at the time
    • Specific histone acetyltransferase at the CXCL1 locus not identified
    • Single-lab in vivo model
  27. 2024 Medium

    Multiple tumor contexts converge on CXCL1 as a feed-forward node remodeling immune and stromal microenvironments through additional inducers (ApoE-LDLR-NF-κB, METTL3-m6A-BHLHE41, ROS-JAK2-STAT1, CD147-PI3K/AKT, Col1-CXCR2-STAT3) and effectors (VEGF-A angiogenesis, MMP-13 invasion).

    Evidence Genetic knockouts, knockdowns, m6A-seq, pathway inhibition, and in vivo tumor/fibrosis/pregnancy models across colorectal, pancreatic, esophageal, hepatic, bladder, ovarian/endometrial systems

    PMID:18451219 PMID:22615136 PMID:29642635 PMID:31438997 PMID:33770315 PMID:34049975 PMID:35700773 PMID:37851572

    Open questions at the time
    • Each inducing pathway shown in a single context/lab
    • Whether these converge on the same promoter elements not unified

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the monomer-dimer-heterodimer equilibrium, dual GAG domains, and CXCR2 occupancy are spatiotemporally coordinated to generate tissue-specific chemotactic gradients in vivo remains unresolved.
  • No in vivo measurement of local oligomeric state and GAG occupancy
  • Structural model of the receptor-bound dimer/heterodimer lacking
  • Mechanism integrating biophysical parameters with directed migration undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 4 GO:0060089 molecular transducer activity 4 GO:0008289 lipid binding 2
Localization
GO:0005576 extracellular region 3
Pathway
R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-162582 Signal Transduction 3
Partners
ACKR1CXCL2CXCR1CXCR2

Evidence

Reading pass · 40 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1989 Human umbilical vein endothelial cells synthesize and secrete CXCL1/MGSA; expression is strongly induced by IL-1, TNF, LPS, and thrombin in a dose- and time-dependent manner independent of new protein synthesis. TPA mimics induction, suggesting protein kinase C mediates the response. Exogenous CXCL1 induces its own gene expression in endothelial cells, demonstrating an autocrine mechanism. Northern blot, ELISA, TPA/PKC pharmacology, recombinant cytokine stimulation of primary HUVEC cultures The EMBO journal Medium 2670560
1990 Recombinant CXCL1/MGSA purified from mammalian expression is mitogenically active on Hs294T melanoma cells, is devoid of glycosylation/sulfation/phosphorylation, and its two C-terminal amino acids are proteolytically removed (71 rather than 73 residues). The protein competes with IL-8 for binding to neutrophil receptors and exhibits neutrophil chemotactic activity equivalent to IL-8. Recombinant expression, mass spectrometry, NH2-terminal sequencing, receptor competition binding, neutrophil chemotaxis assay Biochemistry High 2271650
1990 CXCL1/MGSA stimulates proliferation of normal human epidermal melanocytes as a single agent (ED50 ~0.2 ng/ml). CXCL1 mRNA is constitutively expressed in the absence of exogenous growth factors in nevus and melanoma cultures but is minimal in normal melanocytes, indicating that constitutive autocrine CXCL1 signaling correlates with partial freedom from growth control in transformed melanocytes. Growth assays, Northern blot/mRNA detection, immunoprotein analysis with/without serum Journal of cellular biochemistry Medium 2095366
1991 Overexpression of CXCL1/MGSA in immortalized mouse melanocytes (melan-a cells) confers anchorage-independent growth (colony formation in soft agar) and tumorigenicity in nude mice, demonstrating that CXCL1 can drive oncogenic transformation. Tumor cells expressing CXCL1 show aneuploidy not seen in the parental line. Stable transfection, soft-agar colony assay, nude mouse xenograft, immunohistochemistry, DNA ploidy analysis Oncogene High 1861861
1993 A novel MGSA/CXCL1-specific receptor was identified on Hs294T melanoma cells (KD ~4 nM, ~60,000 sites/cell) that does not bind IL-8 and mediates dose-dependent cellular proliferation. In U937 monocytic cells, CXCL1 and IL-8 compete for a shared receptor (CXCR2); binding induces rapid Ca2+ flux that cross-desensitizes with IL-8. 125I-MGSA direct binding, Scatchard analysis, receptor cross-competition, Ca2+ flux assay The Journal of biological chemistry High 8380167
1994 Constitutive CXCL1/MGSA-alpha mRNA expression in Hs294T melanoma cells results from 8- to 30-fold elevated basal transcription compared to normal RPE cells. IL-1β/TNF-α increase CXCL1 mRNA primarily through mRNA stabilization in Hs294T cells (half-life extended from 15 min to 6 h), whereas in RPE cells the predominant regulation is transcriptional via NF-κB p50/p65. Mutation of the NF-κB element in the CXCL1 promoter abolishes cytokine-induced transcriptional activation. Northern blot, nuclear run-off transcription assay, CAT reporter + promoter deletion/mutation, gel mobility shift (EMSA), mRNA half-life measurement with actinomycin D Molecular and cellular biology High 8264646
1995 Transcription of CXCL1/MGSA-alpha requires at least three transcription factors forming an enhanceosome-like complex: NF-κB (binding at -78 to -65 bp), Sp1/Sp3 (binding ~42 bp upstream of NF-κB, constitutively required for basal activity), and HMGI(Y) (recognizing an AT-rich motif nested within the NF-κB element). Point mutations eliminating NF-κB or HMGI(Y) binding each reduce both basal and cytokine-induced promoter activity. CAT reporter assay with deletion/point-mutation constructs, EMSA, DNase I footprinting Nucleic acids research High 7479086
1997 Continuous expression of CXCL1/MGSA (alpha, beta, or gamma) in immortalized murine melanocytes results in nearly 100% tumor formation in SCID/nude mice. Anti-CXCL1 antibodies slow or inhibit tumor formation and block the angiogenic response to conditioned medium, indicating a paracrine angiogenic mechanism. Constitutive CXCL1 transcription is regulated by an enhanceosome complex comprising NF-κB, HMGI(Y), IUR-binding factor, and Sp1 elements; shortened IκB half-life in melanoma cells promotes constitutive NF-κB nuclear localization. SCID/nude mouse xenograft, antibody neutralization, conditioned medium angiogenesis assay, RT-PCR, ELISA, immunohistochemistry Journal of leukocyte biology High 9365113
1997 CXCL1/MGSA promotes keratinocyte proliferation (maximum 2.6-fold at 10 ng/ml, ED50 ~0.2 ng/ml), increases S-phase fraction, upregulates integrin alpha-6 expression, and accelerates wound epithelialization in an athymic mouse split-thickness graft model. CXCL1 also reduces wound contraction. Keratinocyte proliferation assay, DNA content/cell cycle analysis, integrin flow cytometry, in vivo mouse wound healing model with topical CXCL1 Archives of dermatological research Medium 9143736
1999 Hs294T melanoma cells have constitutively elevated IκB kinase (IKK) activity with increased IκB-alpha phosphorylation at Ser-32 and enhanced degradation, leading to elevated nuclear NF-κB (p50/p65) that drives increased basal CXCL1 transcription. Co-transfection of dominant-negative IKK-alpha or IκB-alpha wild-type/mutants reduces basal CXCL1 promoter-reporter activity, establishing IKK→NF-κB as the mechanism for elevated CXCL1 in melanoma. IKK immunoprecipitation-kinase assay, phospho-specific IκB-alpha antibody, proteasome inhibitor treatment, CXCL1 promoter-luciferase reporter co-transfection with dominant-negative constructs Cancer research High 10096573
2000 CXCL1/MGSA-expressing melanocytes exhibit elevated AP-1 activity, upregulation of M-Ras/R-Ras3 at mRNA and protein levels, and increases in K-Ras and N-Ras protein. The transformation-inducing effect of CXCL1 requires an intact ELR motif and is blocked by dominant-negative M-Ras; overexpression of M-Ras alone mimics CXCL1-induced soft-agar transformation, placing Ras downstream of CXCL1 signaling in melanocyte transformation. Differential display, Western blot, AP-1-luciferase reporter, dominant-negative and constitutively active M-Ras overexpression, ELR-mutant CXCL1 expression, soft-agar assay Oncogene High 11030154
2000 Tumor-forming capacity of CXCL1-expressing melanocytes requires receptor activation via the ELR motif: melan-a cells expressing ELR-mutant CXCL1 (compromised CXCR2 affinity) show markedly impaired tumorigenicity in athymic mice compared to wild-type CXCL1-expressing clones. Anti-CXCL1 antiserum reduces tumor growth and angiogenic activity in vivo, supporting both paracrine (angiogenic) and autocrine (melanocyte growth) mechanisms. Athymic nude mouse xenograft with ELR-mutant CXCL1 clones, SCID mouse antiserum treatment, angiogenesis assay Journal of leukocyte biology High 10647998
2002 CXCL1-induced CXCR2-mediated chemotaxis requires activation of the cdc42–PAK1 signaling cascade. CXCL1 induces cdc42 and PAK1 activation in CXCR2-expressing HEK293 cells; dominant-negative ERK or MEK inhibitor PD98059 does not affect PAK1 activation or chemotaxis, showing PAK1 acts independently of ERK1/2. PAK1 activation is required for chemotaxis but not for CXCL1-induced intracellular Ca2+ mobilization. Dominant-negative expression constructs, kinase activity assay, Ca2+ mobilization assay, chemotaxis (Boyden chamber) assay, MEK inhibitor pharmacology Biochemistry High 12033944
2005 Hyaluronan dodecasaccharides (HA12) selectively upregulate CXCL1/GRO1 gene expression in endothelial cells via CD44. Neutralizing anti-CXCL1 antibody inhibits HA12-induced endothelial cell capillary sprouting in 3D collagen gels, establishing CXCL1 as a required mediator of HA12-driven angiogenic morphogenesis. Blocking CD44 function abolishes HA12-induced CXCL1 upregulation and morphogenesis. Microarray, neutralizing antibody inhibition of 3D tube formation assay, CD44-blocking antibody treatment The Journal of biological chemistry Medium 15843382
2013 The CXCL1 dimer (engineered via disulfide trapping) binds CXCR2 with nanomolar affinity and acts as a potent agonist comparable to the monomer. Both monomer and dimer engage the CXCR2 N-terminal domain with essentially conserved binding interactions. This contrasts with CCL2/CCL4 dimers (inactive) and the CXCL8 dimer (marginally active), demonstrating that the dimer is a functionally active form unique among characterized chemokines for CXCR2. Disulfide-trapped dimer construction, CXCR2 binding assays, cellular agonist assays (Ca2+ flux, receptor internalization), NMR-based binding characterization of N-terminal domain interaction The Journal of biological chemistry High 23479735
2013 IL-1β-mediated induction of CXCL1 in pancreatic β-cells requires NF-κB (p65/p50) binding to consensus κB elements in the CXCL1 proximal promoter, serine-phosphorylated STAT1 binding to the CXCL1 promoter, and specific histone H3 modifications (in a time frame congruent with transcription factor recruitment). Mutation of the NF-κB consensus element reduces IL-1β-induced transcription. CXCL1 protein stimulates integrin expression on human neutrophil surfaces. Promoter mutation, chromatin immunoprecipitation (ChIP) for p65/p50/STAT1/RNA Pol II, histone H3 modification analysis, ELISA, flow cytometry American journal of physiology. Endocrinology and metabolism High 24280128
2015 CXCL1 contains two distinct, non-overlapping glycosaminoglycan (GAG)-binding domains identified by NMR: an α-domain (N-loop and C-helix residues, shared with CXCL8) and a novel β-domain (N-terminus, 40s turn, third β-strand). The CXCL1 dimer is the high-affinity GAG ligand. β-domain mutagenesis eliminates β-domain GAG binding without perturbing α-domain binding. Receptor-binding residues substantially overlap with GAG-binding residues, and GAG-bound CXCL1 fully occludes CXCR2 access. NMR spectroscopy (chemical shift mapping with heparin oligosaccharides), site-directed mutagenesis, GAG binding assays The Journal of biological chemistry High 26721883
2016 In vivo neutrophil recruitment by CXCL1 requires both CXCR2 receptor activation and GAG-binding activity. Lysine/arginine-to-alanine mutations in either the α- or β-GAG-binding domain reduce heparin affinity and peritoneal neutrophil recruitment. Wild-type CXCL1 is more active than monomers or dimers alone, indicating synergistic interactions between forms. A residue involved in both GAG binding and receptor signaling shows the greatest reduction in recruitment. Site-directed mutagenesis, heparin affinity assay, mouse peritoneal neutrophil recruitment model, trapped monomer/dimer variants Scientific reports High 27625115
2016 CXCL1/CXCR2 activation in macrophages activates NLRP3 inflammasome via a protein kinase C μ (PKCμ)-dependent integrin-linked kinase (ILK) pathway. Blocking CXCL1/CXCL2 in vivo reduces M. tuberculosis-induced bioactive IL-1β production. siRNA knockdown or pharmacologic inhibition of ILK or PKCμ abolishes CXCL1-mediated inflammasome activation and IL-1β production. siRNA knockdown, pharmacologic inhibition, in vivo carrageenan inflammation models, NLRP3 inflammasome activation assays, M. tuberculosis infection model Journal of immunology High 28739876
2016 Mtb-triggered Hippo signaling (MST1/2) upregulates CXCL1 and CXCL2 expression and secretion in macrophages via a TLR2–IRAK1/4–MST1/2–IRF3 axis (LATS1-independent, non-canonical Hippo pathway). Silencing MST1/2 significantly reduces Mtb-induced CXCL1/2 secretion. Secreted CXCL1/2 act in paracrine to induce anti-microbial peptides (beta-defensins), iNOS, NOX2 and pro-inflammatory molecules. siRNA-mediated MST1/2 knockdown, pharmacologic TLR2/IRAK inhibition, ELISA, co-culture paracrine assays, M. tuberculosis infection model Scientific reports Medium 27883091
2018 CXCL1 produced mainly by TNF-stimulated endothelial cells and pericytes supports luminal and sub-endothelial neutrophil crawling during transmigration. CXCL2 (from neutrophils) bound to ACKR1 at endothelial junctions is required for endothelial junction breaching. These two chemokines act in a non-redundant, sequential manner to guide neutrophils through venular walls as governed by their distinct cellular sources. Confocal intravital microscopy in mouse cremaster muscle, CXCL1/CXCL2 knockout mice, ACKR1-deficient mice, cell-specific reporter systems Immunity High 30446388
2019 Mechanical stretch of liver sinusoidal endothelial cells (LSECs) upregulates CXCL1 expression via integrin-dependent activation of Notch1 transcription factor and interaction with the mechanosensitive Piezo calcium channel. LSEC-derived CXCL1 recruits neutrophils into the sinusoidal lumen, promoting sinusoidal microthrombi (NETs) and portal hypertension. LSEC-specific Notch1 deletion reduces CXCL1-mediated neutrophil recruitment. Flexcell mechanical stretch device, microarray/RNA-seq, Notch1iΔEC knockout mice, intravital liver imaging, NE-/- and Pad4-/- knockout mice, portal pressure measurement Gastroenterology High 30872106
2019 NFκB-dependent CXCL1 expression in spinal astrocytes signals to CXCR2 on PAG neurons to mediate descending pain facilitation in bone cancer pain. BAY11-7082 (NF-κB inhibitor) micro-injected into vlPAG attenuates pain and reduces CXCL1; CXCL1 neutralizing antibody attenuates mechanical allodynia; CXCR2 antagonist SB225002 completely blocks CXCL1-induced allodynia. CXCL1 co-localizes with astrocyte marker GFAP, while CXCR2 localizes to neurons. Intrathecal/micro-injection of inhibitors and neutralizing antibodies, immunohistochemical co-localization, Western blot, behavioral pain testing Journal of neuroinflammation Medium 30606213
2019 CXCL1/CXCR2 signaling mediates vaso-occlusive crisis (VOC) in sickle cell disease. Recombinant CXCL1 administration alone is sufficient to induce acute VOC (leukocyte recruitment, red blood cell capture, reduced venular flow, shortened survival) in humanized SCD mice. CXCR2 blockade prevents HTR-elicited acute VOC and prolongs survival. Humanized SCD mouse model, recombinant CXCL1 administration, CXCR2 blockade, intravital microscopy The Journal of clinical investigation High 21383500
2020 CXCL1 is produced by astrocytes in response to HSV-1 infection and by both astrocytes and neurons in response to IL-1α; it is the critical ligand for CXCR2-dependent neutrophil transendothelial migration and blood-brain barrier permeability in viral encephalitis. Cxcr2-deficient mice show markedly reduced neutrophil recruitment and BBB permeability without affecting viral load, placing CXCL1-CXCR2 specifically in the neutrophil-mediated pathological arm. Cxcr2 knockout mouse model, HSV-1 encephalitis model, intravital/confocal imaging, BBB permeability assay, viral titer measurement, cell-type specific cytokine production analysis Cell reports High 32937134
2020 Mouse Cxcl1 and Cxcl2 monomers and dimers differ in CXCR2 G-protein and β-arrestin activity (Cxcl2 variants are more potent for CXCR2 activity) and in heparan sulfate binding affinity (Cxcl1 and dimers bind more avidly). In vivo peritoneal neutrophil recruitment cannot be explained by either Cxcr2 activity or GAG binding alone; the relationship is complex and dose/time-point dependent, suggesting that the monomer-dimer equilibrium coordinates recruitment. CXCR2 G protein and β-arrestin cellular assays, heparan sulfate binding assays, mouse peritoneal neutrophil recruitment, Cxcr2/CD11b flow cytometry, trapped dimer variants Journal of leukocyte biology High 32881070
2021 ApoE induces pancreatic tumor cell expression of Cxcl1 and Cxcl5 through LDL receptor and NF-κB signaling, thereby promoting immune suppression (CD8+ T cell exclusion) in PDAC. ApoE-knockout mice with orthotopic tumors show increased CD8+ T cells and reduced tumor growth. Orthotopic implantation in wild-type vs ApoE-knockout mice, CyTOF mass cytometry, LDL receptor pathway inhibition, NF-κB pathway analysis, histology Cancer research Medium 34049975
2022 METTL3 promotes CXCL1 expression in colorectal cancer cells via an m6A-BHLHE41 axis: METTL3 promotes BHLHE41 expression in an m6A-dependent manner, and BHLHE41 subsequently induces CXCL1 transcription to enhance MDSC migration. BHLHE41 depletion abolishes the effect of METTL3 on CXCL1-driven MDSC migration. CXCR2 inhibitor SB265610 blocks MDSC migration in vitro. m6A sequencing, RNA-seq, cytokine arrays, siRNA knockdown, CXCR2 inhibitor, syngeneic mouse models, Mettl3 knockout mice, CD34+ humanized mice Gastroenterology High 35700773
2023 Cell-autonomous CXCL1 in KRAS-TP53 mutant pancreatic cancer drives spatial T-cell exclusion via CXCR2+ neutrophilic MDSCs. Silencing CXCL1 in KPC cells reprograms neutrophil trafficking to overcome T-cell exclusion. Neutrophil-derived TNF acts as a central regulator via transmembrane TNF-TNFR2 interactions to sustain feed-forward CXCL1 overproduction from tumor cells and cancer-associated fibroblasts (CAFs), and drives inflammatory CAF polarization. TNFR2 inhibition disrupts this circuit and improves chemotherapy sensitivity. Imaging mass cytometry, shRNA silencing of Cxcl1 in KPC cells, KPC mouse model, TNFR2 inhibition, bone marrow transplant, co-culture experiments Cancer discovery High 36946782
2023 The Cxcl1-Cxcl2 heterodimer is a more potent neutrophil chemoattractant than either homodimer or monomer in vivo. Heterodimer binds glycosaminoglycans with higher affinity than Cxcl1 or Cxcl2, but shows dampened CXCR2 receptor activity. Optimal GAG interactions and dampened receptor activity act together to promote robust neutrophil recruitment. Engineered heterodimer, CXCR2 cellular activity assays, heparan sulfate binding assay, mouse peritoneal neutrophil recruitment, flow cytometry of Cxcr2/CD11b on recruited neutrophils Journal of leukocyte biology High 37625009
2019 Spinal CXCL1/CXCR2 signaling drives paclitaxel-induced neuropathic pain via a PI3Kγ-dependent downstream pathway. Intrathecal (spinal) but not systemic blockade of CXCL1 (neutralizing antibody) or CXCR2 (SB225002) or PI3Kγ inhibition consistently reduces paclitaxel-induced mechanical hypersensitivity in mice. CXCL1 is elevated in dorsal root ganglion and spinal cord after paclitaxel treatment. Intrathecal microinjection of anti-CXCL1 antibody and CXCR2 antagonist, PI3Kγ inhibitors (AS605240, wortmannin), behavioral pain testing, ELISA/Western blot Neuropharmacology Medium 30991054
2019 Topoisomerase inhibitors promote CXCL1 expression and cancer cell migration via a ROS→PTP1B oxidation→JAK2→STAT1→CXCL1 pathway. JAK2 or STAT1 siRNA knockdown or pharmacologic inhibition abrogates topoisomerase inhibitor-induced CXCL1 and cell motility. Reduced glutathione (GSH) reverses ROS-induced JAK2-STAT1 activation and CXCL1 expression. Transwell migration assay, mass spectrometry (conditioned medium), siRNA knockdown, JAK2/STAT1 inhibitors, GSH treatment, Western blot for pJAK2/pSTAT1 Journal of experimental & clinical cancer research Medium 31438997
2019 TLR4 signaling in DRG neurons induces CXCL1 expression after MOG35-55 immunization; gene silencing of TLR4 or CXCL1 in DRG neurons significantly attenuates neutrophil accumulation in the DRG and mechanical allodynia during the preclinical phase of EAE. MOG35-55 directly induces CXCL1 protein in primary cultured DRG neurons via TLR4. In vivo gene silencing (siRNA), primary cultured DRG neuron stimulation, Western blot, behavioral pain testing, histology Scientific reports Medium 31427756
2022 Spinal microglia-derived TNF activates astrocytic JNK MAPK signaling to drive CXCL1 expression in burn pain. Intrathecal TNF injection causes astrocyte activation and CXCL1 upregulation via JNK; thalidomide (TNF inhibitor) suppresses astrocyte activation and pain. CXCR2 antagonist SB225002 blocks CXCL1 biological activity and attenuates mechanical allodynia/thermal hyperalgesia. Second-degree burn pain mouse model, intrathecal TNF injection, TNF inhibitor thalidomide, p38/JNK MAPK inhibitors, CXCR2 antagonist, Western blot, immunofluorescence Brain, behavior, and immunity Medium 35143878
2018 CD147 overexpression in activated hepatic stellate cells (HSCs) upregulates CXCL1 secretion via the PI3K/AKT signaling pathway; secreted CXCL1 promotes HSC activation in an autocrine manner. PI3K/AKT inhibitor suppresses CD147-induced CXCL1 expression. CD147-specific deletion in HSCs reduces CCl4-induced liver fibrosis and CXCL1 levels. CD147 conditional knockout mice, CXCL1 overexpression, PI3K/AKT inhibitor, CCl4 liver fibrosis model, ELISA, Western blot International journal of molecular sciences Medium 29642635
2008 CXCL1 is preferentially secreted by highly invasive bladder carcinoma cell lines and modulates their invasive ability in vitro. CXCL1 regulates matrix metalloproteinase-13 (MMP-13) expression in bladder cancer cells, providing a mechanism linking CXCL1 to matrix remodeling and invasion. Shotgun proteomics of secreted proteins, invasion assay, MMP-13 expression analysis by in vitro treatment with recombinant CXCL1 Clinical cancer research Medium 18451219
2021 CXCL1 stimulates decidual angiogenesis during early pregnancy via the VEGF-A/VEGFR2 pathway. Exogenous CXCL1 promotes endothelial cell proliferation, migration, and tube formation in HUVEC-HTR8/SVneo co-culture, effects blocked by CXCL1-neutralizing antibody or CXCR2 inhibitor SB265610. CXCL1 increases VEGF-A expression in HUVEC cells; in vivo CXCL1 neutralization reduces decidual CD34+ vascularity and VEGF-A/VEGFR2 expression. HUVEC/trophoblast co-culture tube formation assay, CXCL1-neutralizing antibody, CXCR2 inhibitor, in-cell western VEGF-A analysis, mouse pregnancy model with in vivo antibody injection, immunohistochemistry Molecular and cellular biochemistry Medium 33770315
2024 Acetyl-CoA accumulation in hepatocellular carcinoma cells induces H3 acetylation-dependent transcriptional upregulation of CXCL1, which recruits tumor-associated neutrophils and promotes NET formation via CXCR2, leading to HCC metastasis. CXCL1 was identified as the critical mediator by cytokine microarray and ELISA, linking metabolic reprogramming to immune microenvironment remodeling. Cytokine microarray, ELISA, orthotopic xenograft models, H3 acetylation ChIP, CXCL1 knockdown, CXCR2 inhibition, NET formation assay Cancer letters Medium 38670307
2023 Collagen type 1 (Col1) from cancer-associated fibroblasts induces CXCL1 secretion in esophageal cancer tumor cells; secreted CXCL1 activates CAFs via CXCR2-STAT3 signaling, establishing a positive feedback loop that promotes radioresistance. Directly inhibiting tumor-cell-derived CXCL1 or the CXCL1-CXCR2 pathway restores radiosensitivity in vivo. Patient-derived xenografts, RNA-seq, cytokine arrays, single-cell RNA-seq, CXCL1 knockdown, CXCR2-STAT3 pathway inhibition, in vivo radioresistance model Cell reports Medium 37851572
2012 Progesterone and calcitriol suppress CXCL1 and CXCL2 expression in ovarian/endometrial cancer cells through inhibition of IκBα phosphorylation and NF-κB activation. NF-κB knockdown reduces CXCL1/2; IκBα silencing increases CXCL1/2 via elevated NF-κB-p65; the inhibitory effect of progesterone/calcitriol is abolished in IκBα-knockdown cells, establishing an NF-κB-dependent mechanism. RT-PCR cytokine array, siRNA knockdown of NF-κB and IκBα, ELISA, Western blot for IκBα phosphorylation Journal of cellular biochemistry Medium 22615136

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 A CXCL1 paracrine network links cancer chemoresistance and metastasis. Cell 900 22770218
2018 Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis. Immunity 286 30446388
2016 Chemokine CXCL1 mediated neutrophil recruitment: Role of glycosaminoglycan interactions. Scientific reports 276 27625115
2020 Fusobacterium nucleatum host-cell binding and invasion induces IL-8 and CXCL1 secretion that drives colorectal cancer cell migration. Science signaling 269 32694172
2018 CXCL1-CXCR2 axis mediates angiotensin II-induced cardiac hypertrophy and remodelling through regulation of monocyte infiltration. European heart journal 249 29514257
2002 Role of CXCL1 in tumorigenesis of melanoma. Journal of leukocyte biology 239 12101257
2022 METTL3 Inhibits Antitumor Immunity by Targeting m6A-BHLHE41-CXCL1/CXCR2 Axis to Promote Colorectal Cancer. Gastroenterology 211 35700773
2019 Mechanical Stretch Increases Expression of CXCL1 in Liver Sinusoidal Endothelial Cells to Recruit Neutrophils, Generate Sinusoidal Microthombi, and Promote Portal Hypertension. Gastroenterology 205 30872106
1997 Mechanism and biological significance of constitutive expression of MGSA/GRO chemokines in malignant melanoma tumor progression. Journal of leukocyte biology 163 9365113
2021 Apolipoprotein E Promotes Immune Suppression in Pancreatic Cancer through NF-κB-Mediated Production of CXCL1. Cancer research 152 34049975
2013 NF-κB and STAT1 control CXCL1 and CXCL2 gene transcription. American journal of physiology. Endocrinology and metabolism 149 24280128
2000 The tumorigenic and angiogenic effects of MGSA/GRO proteins in melanoma. Journal of leukocyte biology 139 10647998
2016 CXCL1 mediates obesity-associated adipose stromal cell trafficking and function in the tumour microenvironment. Nature communications 138 27241286
1989 Expression and secretion of gro/MGSA by stimulated human endothelial cells. The EMBO journal 138 2670560
2017 CXCL1/CXCR2 signaling in pathological pain: Role in peripheral and central sensitization. Neurobiology of disease 130 28587921
2017 CXCL1 and CXCL2 Regulate NLRP3 Inflammasome Activation via G-Protein-Coupled Receptor CXCR2. Journal of immunology (Baltimore, Md. : 1950) 129 28739876
2022 CXCL1: Gene, Promoter, Regulation of Expression, mRNA Stability, Regulation of Activity in the Intercellular Space. International journal of molecular sciences 125 35054978
2022 PMN-MDSCs accumulation induced by CXCL1 promotes CD8+ T cells exhaustion in gastric cancer. Cancer letters 125 35176418
2020 Neutrophil recruitment by chemokines Cxcl1/KC and Cxcl2/MIP2: Role of Cxcr2 activation and glycosaminoglycan interactions. Journal of leukocyte biology 119 32881070
2020 Astrocyte- and Neuron-Derived CXCL1 Drives Neutrophil Transmigration and Blood-Brain Barrier Permeability in Viral Encephalitis. Cell reports 118 32937134
2023 Cell-Autonomous Cxcl1 Sustains Tolerogenic Circuitries and Stromal Inflammation via Neutrophil-Derived TNF in Pancreatic Cancer. Cancer discovery 116 36946782
2011 Overexpression of CXCL1 and its receptor CXCR2 promote tumor invasion in gastric cancer. Annals of oncology : official journal of the European Society for Medical Oncology 112 21343381
2006 Role for CXCR2 and CXCL1 on glia in multiple sclerosis. Glia 110 16086366
2021 Regulation of tumor immune suppression and cancer cell survival by CXCL1/2 elevation in glioblastoma multiforme. Science advances 103 33571109
2005 Hyaluronan fragments induce endothelial cell differentiation in a CD44- and CXCL1/GRO1-dependent manner. The Journal of biological chemistry 102 15843382
2010 Aberrant expression of selectin E, CXCL1, and CXCL13 in chronic endometritis. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 100 20495539
1991 Effects of MGSA/GRO alpha on melanocyte transformation. Oncogene 98 1861861
2024 H3K18 lactylation-mediated VCAM1 expression promotes gastric cancer progression and metastasis via AKT-mTOR-CXCL1 axis. Biochemical pharmacology 97 38461905
2008 Secreted CXCL1 is a potential mediator and marker of the tumor invasion of bladder cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 96 18451219
2019 Crosstalk between NFκB-dependent astrocytic CXCL1 and neuron CXCR2 plays a role in descending pain facilitation. Journal of neuroinflammation 89 30606213
1995 HMGI(Y) and Sp1 in addition to NF-kappa B regulate transcription of the MGSA/GRO alpha gene. Nucleic acids research 87 7479086
1990 Recombinant expression, biochemical characterization, and biological activities of the human MGSA/gro protein. Biochemistry 84 2271650
2014 Increased serum CXCL1 and CXCL5 are linked to obesity, hyperglycemia, and impaired islet function. The Journal of endocrinology 82 24928936
2019 RIP3 promotes colitis-associated colorectal cancer by controlling tumor cell proliferation and CXCL1-induced immune suppression. Theranostics 81 31281505
1990 Characterization of the role of melanoma growth stimulatory activity (MGSA) in the growth of normal melanocytes, nevocytes, and malignant melanocytes. Journal of cellular biochemistry 81 2095366
1999 Elevated constitutive IkappaB kinase activity and IkappaB-alpha phosphorylation in Hs294T melanoma cells lead to increased basal MGSA/GRO-alpha transcription. Cancer research 77 10096573
2022 The Potential Importance of CXCL1 in the Physiological State and in Noncancer Diseases of the Cardiovascular System, Respiratory System and Skin. International journal of molecular sciences 72 36613652
2009 Deletion of methylglyoxal synthase gene (mgsA) increased sugar co-metabolism in ethanol-producing Escherichia coli. Biotechnology letters 72 19458924
2021 Aiduqing formula inhibits breast cancer metastasis by suppressing TAM/CXCL1-induced Treg differentiation and infiltration. Cell communication and signaling : CCS 71 34461944
2009 Chemokine CXCL1/KC and its receptor CXCR2 are responsible for neutrophil chemotaxis in adenoviral keratitis. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 70 19642907
2011 Lymphatic endothelial cell-secreted CXCL1 stimulates lymphangiogenesis and metastasis of gastric cancer. International journal of cancer 69 21387301
1994 MGSA/GRO transcription is differentially regulated in normal retinal pigment epithelial and melanoma cells. Molecular and cellular biology 67 8264646
2022 Metformin increases natural killer cell functions in head and neck squamous cell carcinoma through CXCL1 inhibition. Journal for immunotherapy of cancer 65 36328378
2016 Mycobacterium tuberculosis-triggered Hippo pathway orchestrates CXCL1/2 expression to modulate host immune responses. Scientific reports 63 27883091
2000 MGSA/GRO-mediated melanocyte transformation involves induction of Ras expression. Oncogene 63 11030154
2023 Chronic psychological stress promotes breast cancer pre-metastatic niche formation by mobilizing splenic MDSCs via TAM/CXCL1 signaling. Journal of experimental & clinical cancer research : CR 58 37210553
2013 Chemokine CXCL1 dimer is a potent agonist for the CXCR2 receptor. The Journal of biological chemistry 57 23479735
2024 CD276 regulates the immune escape of esophageal squamous cell carcinoma through CXCL1-CXCR2 induced NETs. Journal for immunotherapy of cancer 56 38724465
2023 A polysaccharide NAP-3 from Naematelia aurantialba: Structural characterization and adjunctive hypoglycemic activity. Carbohydrate polymers 54 37479455
2011 Catabolic regulation analysis of Escherichia coli and its crp, mlc, mgsA, pgi and ptsG mutants. Microbial cell factories 54 21831320
2020 Promising targets of chrysin and daidzein in colorectal cancer: Amphiregulin, CXCL1, and MMP-9. European journal of pharmacology 53 33249075
2012 Progesterone and calcitriol attenuate inflammatory cytokines CXCL1 and CXCL2 in ovarian and endometrial cancer cells. Journal of cellular biochemistry 47 22615136
2010 NOV/CCN3 upregulates CCL2 and CXCL1 expression in astrocytes through beta1 and beta5 integrins. Glia 46 20648642
1993 Purification, receptor binding analysis, and biological characterization of human melanoma growth stimulating activity (MGSA). Evidence for a novel MGSA receptor. The Journal of biological chemistry 46 8380167
2019 Spinal blockage of CXCL1 and its receptor CXCR2 inhibits paclitaxel-induced peripheral neuropathy in mice. Neuropharmacology 45 30991054
2017 Preclinical chorioamnionitis dysregulates CXCL1/CXCR2 signaling throughout the placental-fetal-brain axis. Experimental neurology 44 29117499
2003 Fine tuning the transcriptional regulation of the CXCL1 chemokine. Progress in nucleic acid research and molecular biology 44 14510072
2023 Vascular cell-adhesion molecule 1 (VCAM-1) regulates JunB-mediated IL-8/CXCL1 expression and pathological neovascularization. Communications biology 43 37179352
2022 CXCL1 promotes colon cancer progression through activation of NF-κB/P300 signaling pathway. Biology direct 43 36434686
2019 The chemokine CXCL1 and its receptor CXCR2 contribute to chronic stress-induced depression in mice. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 43 31034777
2015 CXCL1/MGSA Is a Novel Glycosaminoglycan (GAG)-binding Chemokine: STRUCTURAL EVIDENCE FOR TWO DISTINCT NON-OVERLAPPING BINDING DOMAINS. The Journal of biological chemistry 43 26721883
2023 The Clinical Significance and Role of CXCL1 Chemokine in Gastrointestinal Cancers. Cells 40 37408240
2022 CXCL1-CXCR2 signalling mediates hypertensive retinopathy by inducing macrophage infiltration. Redox biology 40 35981418
2019 Monoclonal Antibody against CXCL1 (HL2401) as a Novel Agent in Suppressing IL6 Expression and Tumoral Growth. Theranostics 40 30809313
2021 CXCL1: A new diagnostic biomarker for human tuberculosis discovered using Diversity Outbred mice. PLoS pathogens 38 34403447
2018 CD147 Promotes CXCL1 Expression and Modulates Liver Fibrogenesis. International journal of molecular sciences 38 29642635
2005 Functional overlap between RecA and MgsA (RarA) in the rescue of stalled replication forks in Escherichia coli. Genes to cells : devoted to molecular & cellular mechanisms 38 15743409
2011 CXCL1 and its receptor, CXCR2, mediate murine sickle cell vaso-occlusion during hemolytic transfusion reactions. The Journal of clinical investigation 37 21383500
2023 Collagen 1-mediated CXCL1 secretion in tumor cells activates fibroblasts to promote radioresistance of esophageal cancer. Cell reports 36 37851572
1997 Role of melanoma growth stimulatory activity (MGSA/gro) on keratinocyte function in wound healing. Archives of dermatological research 35 9143736
2023 The role of CXCL1/CXCR2 axis in neurological diseases. International immunopharmacology 34 37247498
2002 PAK1 kinase is required for CXCL1-induced chemotaxis. Biochemistry 34 12033944
1993 Localization of MGSA/GRO protein in cutaneous lesions. Journal of cutaneous pathology 33 8366215
2024 Acetyl-CoA metabolic accumulation promotes hepatocellular carcinoma metastasis via enhancing CXCL1-dependent infiltration of tumor-associated neutrophils. Cancer letters 31 38670307
2011 Structure and biochemical activities of Escherichia coli MgsA. The Journal of biological chemistry 31 21297161
2020 CXCL1/CXCR2 Paracrine Axis Contributes to Lung Metastasis in Osteosarcoma. Cancers 30 32079335
2019 Topoisomerase inhibitors promote cancer cell motility via ROS-mediated activation of JAK2-STAT1-CXCL1 pathway. Journal of experimental & clinical cancer research : CR 30 31438997
2017 CXCL1 Inhibition Regulates UVB-Induced Skin Inflammation and Tumorigenesis in Xpa-Deficient Mice. The Journal of investigative dermatology 30 28528167
2014 CXCL1 gene silencing in skin using liposome-encapsulated siRNA delivered by microprojection array. Journal of controlled release : official journal of the Controlled Release Society 30 25192942
2023 Dysregulation of CXCL1 Expression and Neutrophil Recruitment in Insulin Resistance and Diabetes-Related Periodontitis in Male Mice. Diabetes 29 37058471
2021 CXCL1 stimulates decidual angiogenesis via the VEGF-A pathway during the first trimester of pregnancy. Molecular and cellular biochemistry 29 33770315
2005 Endothelin-1 induces CXCL1 and CXCL8 secretion in human melanoma cells. The Journal of investigative dermatology 27 16098041
2024 M2 macrophages promote PD-L1 expression in triple-negative breast cancer via secreting CXCL1. Pathology, research and practice 26 39003998
2022 Spinal microglia-derived TNF promotes the astrocytic JNK/CXCL1 pathway activation in a mouse model of burn pain. Brain, behavior, and immunity 26 35143878
2022 Hepatic stellate cell-released CXCL1 aggravates HCC malignant behaviors through the MIR4435-2HG/miR-506-3p/TGFB1 axis. Cancer science 25 36169092
2019 A TLR-CXCL1 pathway in DRG neurons induces neutrophil accumulation in the DRG and mechanical allodynia in EAE mice. Scientific reports 25 31427756
1993 Expression of three forms of melanoma growth stimulating activity (MGSA)/gro in human retinal pigment epithelial cells. Investigative ophthalmology & visual science 25 8344798
2023 Selective inhibition of HDAC6 promotes bladder cancer radiosensitization and mitigates the radiation-induced CXCL1 signalling. British journal of cancer 24 36810912
2023 circRNF13, a novel N6-methyladenosine-modified circular RNA, enhances radioresistance in cervical cancer by increasing CXCL1 mRNA stability. Cell death discovery 24 37468464
2020 Participation of CXCL1 in the glial cells during neuropathic pain. European journal of pharmacology 24 32119843
2016 Chemokine CXCL1 may serve as a potential molecular target for hepatocellular carcinoma. Cancer medicine 24 27682863
2021 A Role of CXCL1 Drives Osteosarcoma Lung Metastasis via VCAM-1 Production. Frontiers in oncology 23 34760697
2020 A novel approach to treatment of thromboembolic stroke in mice: Redirecting neutrophils toward a peripherally implanted CXCL1-soaked sponge. Experimental neurology 23 32360283
2014 Opioids enhance CXCL1 expression and function after incision in mice. The journal of pain 23 24887006
2024 IGFBP2/ITGA5 promotes gefitinib resistance via activating STAT3/CXCL1 axis in non-small cell lung cancer. Cell death & disease 22 38918360
2020 Cytokines CCL2 and CXCL1 may be potential novel predictors of early bone loss. Molecular medicine reports 22 33173955
2023 Chemokine Cxcl1-Cxcl2 heterodimer is a potent neutrophil chemoattractant. Journal of leukocyte biology 21 37625009
2022 EMT-mediated regulation of CXCL1/5 for resistance to anti-EGFR therapy in colorectal cancer. Oncogene 21 35173310
2021 Chemokine CXCL1 as a potential marker of disease activity in systemic lupus erythematosus. BMC immunology 21 34961474
2024 The Clinical Significance and Involvement in Molecular Cancer Processes of Chemokine CXCL1 in Selected Tumors. International journal of molecular sciences 20 38673949

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