Affinage

Showing CEMIP — KIAA1199 is a alias.

CEMIP

Cell migration-inducing and hyaluronan-binding protein · UniProt Q8WUJ3

Length
1361 aa
Mass
153.0 kDa
Annotated
2026-06-09
100 papers in source corpus 37 papers cited in narrative 37 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

CEMIP (KIAA1199/HYBID) is the principal effector of CD44- and HYAL-independent hyaluronan (HA) depolymerization, binding HA directly and catabolizing it through an endo-β-N-acetylglucosaminidase-dependent clathrin-coated pit pathway in fibroblasts and tumor cells (PMID:23509262). Proper HA-degrading activity depends on intracellular trafficking governed by an N-terminal cleavable signal sequence and an ER-retention motif: in the ER, CEMIP complexes with the chaperone BiP and the calcium channel ITPR3, driving ER calcium leakage that activates PKCα to promote cell migration (PMID:23990668, PMID:23936024). At the cell surface its G8 domain binds ANXA1 to anchor secreted CEMIP for extracellular HA degradation (PMID:33473125), while in endosomes it scaffolds MEK1 to sustain ERK1/2 signaling (PMID:29915160). CEMIP transcription is tightly controlled by inflammatory and hypoxic inputs, including NF-κB downstream of IL-6/IL-1β (PMID:27981209, PMID:33473125), HIF-2α and lactylated HIF1α (PMID:26009875, PMID:36209908), with TGF-β1 suppressing it via PI3K-Akt to govern the molecular weight of newly synthesized HA (PMID:26518873), and ALKBH5-mediated m6A demethylation destabilizing its mRNA (PMID:38199493). Beyond HA turnover, CEMIP functions as a versatile scaffold/adaptor coupling receptor and metabolic signaling: it potentiates EGFR-dependent Src/MEK/ERK signaling and EMT (PMID:25366117), bridges OGT and β-catenin to enhance β-catenin O-GlcNAcylation and glutamine-metabolic reprogramming (PMID:34608265), links MIB1 to GRAF1 for ubiquitin-mediated GRAF1 degradation and CDC42/MAPK-driven EMT (PMID:36849460), binds PP2A to dephosphorylate stathmin and destabilize microtubules (PMID:30202098), and acts as a clathrin adaptor for MHC-I internalization and lysosomal degradation to drive immune evasion (PMID:36596591). In cancer it confers anoikis, hypoxia, and ferroptosis resistance through ATF4/PKCα/Bcl-2/Beclin1 autophagy and ITPR3/CaMKII/NRF2/SLC7A11 axes (PMID:35013120, PMID:35363929), and exosomal CEMIP conditions the brain pre-metastatic niche via endothelial branching and perivascular inflammation (PMID:31685984). Physiologically, CEMIP is required for HA homeostasis in skin, synovium, brain, and bone, where its loss alters antimicrobial defense, dendritic spine density, arthritis susceptibility, and bone mass (PMID:31914398, PMID:30060951, PMID:33473125, PMID:37037828).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2013 High

    Established CEMIP's core molecular identity by showing it mediates HA depolymerization independently of the canonical CD44/HYAL system, resolving the question of how cells catabolize HA through an unexpected clathrin-coated pit route.

    Evidence Glycosaminoglycan-binding assays, siRNA knockdown, cDNA transfection, and clathrin pathway inhibition in skin fibroblasts and disease specimens

    PMID:23509262

    Open questions at the time
    • Catalytic mechanism and whether CEMIP itself or an associated enzyme cleaves HA not fully resolved
    • No structural model of the HA-binding/catalytic site
  2. 2013 High

    Defined the subcellular basis of CEMIP function, showing ER localization, BiP complex formation, and ER-retention-motif-dependent calcium leakage couple CEMIP to PKCα-driven migration, and that trafficking-determining sequences are required for HA depolymerization.

    Evidence SNAP-tag pull-down, FRET calcium measurement, mutagenesis of ER-retention/signal motifs, confocal imaging, and xenografts

    PMID:23936024 PMID:23990668 PMID:24269685

    Open questions at the time
    • How a single protein partitions between ER, surface, and secreted pools is unclear
    • Interaction with ITPR3 from a single proteomics/Co-IP study
  3. 2014 High

    Extended CEMIP beyond HA biology into receptor signaling, identifying it as an NF-κB (BCL-3/p65) target that binds EGFR and Plexin A2 to sustain Src/MEK/ERK signaling, EGF-driven EMT, and protection from Semaphorin 3A death.

    Evidence ChIP, reciprocal Co-IP, siRNA/overexpression, and cell death assays

    PMID:25366117

    Open questions at the time
    • Whether EGFR binding is direct vs. complex-mediated not established
    • Link between HA-degrading activity and receptor scaffolding undefined
  4. 2015 High

    Resolved the hypoxic transcriptional control of CEMIP by showing HIF-2α (not HIF-1α) binds the CEMIP promoter and that Jarid1A-dependent H3K4me3 changes gate expression, positioning CEMIP as a hypoxia-driven migration effector.

    Evidence ChIP, isoform-specific knockdown, H3K4me3 chromatin analysis, and migration assays

    PMID:26009875

    Open questions at the time
    • Reconciliation with later HIF1α-lactylation regulation not addressed
    • Context dependence of HIF isoform usage unknown
  5. 2015 High

    Connected CEMIP to growth-factor and cytokine control of HA size, showing TGF-β1 suppresses HYBID via PI3K-Akt while inducing HAS, determining whether high- or low-MW HA accumulates in normal vs. arthritic synovium.

    Evidence siRNA, pathway-specific inhibitors, HA size-exclusion chromatography, and clinical tissue correlation

    PMID:26518873 PMID:27981209 PMID:28179576

    Open questions at the time
    • Direct transcription factors downstream of these pathways at the CEMIP locus not fully mapped
  6. 2017 High

    Identified CEMIP as a signaling hub in normal cell physiology, controlling Nrg1/MEK/ERK-driven Schwann cell dedifferentiation and myelin clearance, and binding WBP11/PTP4A3 to gate FGFR4/Wnt and EGFR signaling.

    Evidence RNAi, conditional Cre-lox knockout mice, Nrg1 stimulation, Co-IP, and rescue assays

    PMID:28699206 PMID:30626935

    Open questions at the time
    • Mechanism by which CEMIP positions MEK1/ERK in Schwann cells vs. tumor endosomes not unified
    • WBP11/PTP4A3 interactions from a single lab
  7. 2018 High

    Defined endosomal scaffolding of MEK1 as the basis for CEMIP-driven MEK-inhibitor resistance, and revealed multiple scaffold functions (PP2A/stathmin/microtubule destabilization; BiP-promoter-driven hypoxia adaptation) underlying motility and survival.

    Evidence Endosomal fractionation, Co-IP, organoids, in vivo models, phosphatase/microtubule assays, and promoter reporters

    PMID:29505302 PMID:29915160 PMID:30202098 PMID:31303964

    Open questions at the time
    • How CEMIP simultaneously engages PP2A, MEK1, and metabolic programs not integrated
    • Several functional links rest on single-lab data
  8. 2018 Medium

    Demonstrated that CEMIP, not the related TMEM2, is the indispensable HA depolymerase in human fibroblasts, with TMEM2 acting only as an expression modulator, clarifying the division of labor in HA catabolism.

    Evidence Separate siRNA knockdowns, HA depolymerization assays across cell lines

    PMID:30241936

    Open questions at the time
    • Functional knockdown without reconstitution
    • Catalytic vs. trafficking contribution of CEMIP not separated
  9. 2019 High

    Established physiological and microenvironmental roles, showing exosomal CEMIP conditions the brain pre-metastatic niche, and CEMIP drives β-catenin-dependent chondrocyte transdifferentiation, hMSC migration, and metabolic reprogramming.

    Evidence Exosome proteomics with depletion/rescue, RNA-seq, shRNA/CRISPR, signaling rescue, and in vivo metastasis models

    PMID:29505302 PMID:30718510 PMID:30755597 PMID:31685984

    Open questions at the time
    • Mechanism of CEMIP exosomal loading and uptake unknown
    • How extracellular CEMIP acts on recipient cells not defined
  10. 2020 High

    Used knockout mice to define normal physiological requirements for CEMIP-mediated HA turnover in skin antimicrobial defense and brain synaptic structure, and dissected histamine-driven CEMIP induction in skin.

    Evidence Cemip knockout mice with S. aureus challenge, Golgi-Cox/doublecortin staining, and pharmacological H1-receptor/PKCδ/PI3K dissection

    PMID:30060951 PMID:31914398 PMID:31949043

    Open questions at the time
    • Brain phenotype from a single lab without independent replication
    • Causal link between HA accumulation and synaptic deficits incomplete
  11. 2021 High

    Mapped the extracellular HA-degradation machinery to a G8-domain/ANXA1 membrane-tethering mechanism required in vivo for arthritis pathology, and identified CEMIP as an OGT adaptor enabling β-catenin O-GlcNAcylation and glutamine reprogramming.

    Evidence G8-deleted vs. full-length rescue in knockout mice with collagen-induced arthritis; Co-IP of CEMIP-OGT-β-catenin with O-GlcNAcylation assays and metastasis models

    PMID:33473125 PMID:34608265

    Open questions at the time
    • Structural basis of G8/ANXA1 binding not resolved
    • Whether OGT scaffolding and HA degradation are coupled unknown
  12. 2022 High

    Defined CEMIP-driven stress-resistance and immune-evasion mechanisms in cancer: ATF4/PKCα/Bcl-2/Beclin1 autophagy for anoikis resistance, ITPR3/CaMKII/NRF2/SLC7A11 for ferroptosis resistance, clathrin-adaptor-mediated MHC-I degradation, TGFβR-CXCL1/3 neutrophil recruitment, and HIF1α-lactylation-driven angiogenesis.

    Evidence Co-IP, proximity ligation, flow cytometry, CD8+ T-cell cytotoxicity, ChIP/dual-luciferase, and in vivo metastasis models

    PMID:35013120 PMID:35108400 PMID:35363929 PMID:36209908 PMID:36596591

    Open questions at the time
    • Most stress-resistance chains validated in single labs
    • How one scaffold mediates such divergent adaptor functions unresolved
  13. 2023 High

    Established CEMIP as a regulator of ubiquitin-ligase activity—bridging MIB1 to GRAF1 for degradation and blocking FBXW7-mediated c-Myc turnover—and defined skeletal physiology where CEMIP loss increases osteoblast differentiation and bone mass; human TMEM2 was shown to be catalytically inactive unlike mouse.

    Evidence Domain-mapped Co-IP, ubiquitination assays, CDC42/integrin signaling dissection, knockout mice with micro-CT, and HEK293T reconstitution with domain-swap mutagenesis

    PMID:36746261 PMID:36849460 PMID:37037828 PMID:37196767

    Open questions at the time
    • Structural mechanism of scaffold-directed ubiquitination unknown
    • Whether CEMIP's catalytic HA mechanism parallels the TMEM2 GG-domain chemistry untested
  14. 2024 Medium

    Added post-transcriptional control by showing ALKBH5-mediated m6A demethylation destabilizes CEMIP mRNA, linking loss of this regulation to EMT and paclitaxel resistance.

    Evidence mRNA stability assays, ALKBH5 overexpression/knockdown, and drug-sensitivity/EMT marker analysis in NSCLC

    PMID:38199493

    Open questions at the time
    • m6A sites on CEMIP mRNA not mapped
    • Single-lab finding without independent replication

Open questions

Synthesis pass · forward-looking unresolved questions
  • The unifying biochemical question—how CEMIP's intrinsic HA-depolymerizing activity mechanistically relates to its many protein-scaffold/adaptor functions, and what structural features partition it among ER, endosome, surface, and secreted pools—remains open.
  • No high-resolution structure of CEMIP or its catalytic/HA-binding site
  • No reconstituted enzymatic assay distinguishing direct catalysis from adaptor recruitment
  • Mechanism partitioning CEMIP across compartments undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 2 GO:0140098 catalytic activity, acting on RNA 2 GO:0038024 cargo receptor activity 1
Localization
GO:0005576 extracellular region 3 GO:0005783 endoplasmic reticulum 2 GO:0005886 plasma membrane 2 GO:0005768 endosome 1
Pathway
R-HSA-1430728 Metabolism 3 R-HSA-1474244 Extracellular matrix organization 3 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 2 R-HSA-5653656 Vesicle-mediated transport 2
Partners
BIPCTNNB1EGFRITPR3MEK1MIB1OGTPP2A

Evidence

Reading pass · 37 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2013 KIAA1199 (CEMIP) is a hyaluronan-binding protein that mediates hyaluronan depolymerization independently of CD44 and HYAL enzymes. Specific HA binding was demonstrated in glycosaminoglycan-binding assays; knockdown abolished HA degradation by skin fibroblasts; transfection of KIAA1199 cDNA conferred HA catabolism via an endo-β-N-acetylglucosaminidase-dependent mechanism through the clathrin-coated pit pathway. Glycosaminoglycan-binding assay, siRNA knockdown, cDNA transfection, clathrin pathway inhibition Proceedings of the National Academy of Sciences of the United States of America High 23509262
2013 KIAA1199 localizes to the endoplasmic reticulum where it forms a stable complex with the chaperone BiP. An ER-retention motif within KIAA1199 is required for ER localization, BiP interaction, and enhanced cell migration. KIAA1199 mediates ER calcium leakage, and the resultant increase in cytosolic calcium activates protein kinase C alpha (PKCα), promoting cell migration. SNAP-tag pull-down assay, confocal microscopy, FRET-based calcium measurement, spectrofluorometry, Western blotting, mutagenesis of ER-retention motif, siRNA knockdown, in vivo xenograft Journal of the National Cancer Institute High 23990668
2013 The N-terminal 30 amino acids of KIAA1199 function as a cleavable signal sequence required for proper intracellular trafficking and KIAA1199-mediated HA depolymerization. Deletion of the N-terminal portion results in altered intracellular trafficking and loss of HA depolymerization activity. N-terminal deletion constructs, intracellular trafficking assays, HA depolymerization assay FEBS letters Medium 24269685
2013 KIAA1199 is secreted into the extracellular environment by colon cancer cells. It is found in the perinuclear ER and at the cell membrane. Co-immunoprecipitation confirmed interaction with the cell membrane receptor ephrin A2 and with the ER receptor ITPR3 (a key Ca2+ signaling component), linking KIAA1199 to Ca2+ and Wnt/CTNNB1 signaling. Immunostaining, mass spectrometry proteomics, co-immunoprecipitation, transcriptomics PloS one Medium 23936024
2013 Murine Kiaa1199 (mKiaa1199) binds hyaluronan specifically and mediates HA depolymerization via the clathrin-coated pit pathway, consistent with the human ortholog, though slight differences exist in minimum HA degradate sizes. cDNA transfection in cells, glycosaminoglycan-binding assay, HA catabolism assay, clathrin pathway inhibition FEBS open bio Medium 24251095
2014 KIAA1199 is a BCL-3- and p65-dependent NF-κB target gene. It binds Plexin A2 and protects cells from Semaphorin 3A-mediated cell death by promoting EGFR stability and signaling. KIAA1199 is an EGFR-binding protein and its deficiency impairs EGF-dependent Src, MEK1, and ERK1/2 phosphorylations, thereby promoting EGF-mediated EMT. ChIP, co-immunoprecipitation, Western blotting, siRNA knockdown, overexpression, cell death assays Nature communications High 25366117
2014 KIAA1199 interacts with glycogen phosphorylase kinase β-subunit (PHKB) via its C-terminal region, as demonstrated by pull-down assay. Under serum-free conditions, KIAA1199 also interacts with glycogen phosphorylase brain form (PYGB). These interactions promote glycogen breakdown and cancer cell survival. MBP fusion protein pull-down assay, retroviral overexpression, glycogen breakdown assays, cell survival assays Oncotarget Medium 25051373
2015 HIF-2α (but not HIF-1α) directly binds to the hypoxia response element within the CEMIP promoter, driving CEMIP transcription under hypoxic conditions. CEMIP is a downstream effector of HIF-2α-mediated cell migration. CEMIP expression negatively correlates with histone demethylase Jarid1A; low oxygen inhibits Jarid1A, increasing H3K4me3 at the CEMIP promoter. ChIP, promoter binding assay, siRNA knockdown of HIF-1α vs HIF-2α, H3K4me3 chromatin analysis, cell migration assay Oncotarget High 26009875
2015 TGF-β1, bFGF, EGF, and PDGF-BB commonly enhance total HA in skin fibroblasts through HAS up-regulation, but molecular size of newly produced HA depends on HYBID/KIAA1199 expression. TGF-β1 suppresses HYBID expression via PI3K-Akt signaling and stimulates HAS1/2 via MAPK/Smad, resulting in high molecular weight HA. In arthritic synovial fibroblasts, inefficient TGF-β1-mediated suppression of HYBID leads to accumulation of low-MW HA. siRNA knockdown, signaling pathway inhibitors (PI3K, MAPK, Smad), HA size-exclusion chromatography, gene expression analysis, human tissue correlation The Journal of biological chemistry High 26518873
2016 Crohn's Disease fibroblasts overproduce KIAA1199 primarily through an IL-6-driven autocrine mechanism. IL-6 stimulation increases KIAA1199 deposition in the ECM. siRNA silencing of KIAA1199 abrogated HA degradation by colon fibroblasts. Antibody blockade of IL-6 receptors decreased KIAA1199 protein in the ECM. siRNA knockdown, IL-6 receptor antibody blockade, HA degradation biochemical assay, immunoblot, immunostaining of clinical specimens Cellular and molecular gastroenterology and hepatology High 27981209
2017 KIAA1199 expression in cancer cells is induced by pro-inflammatory cytokine IL-1β and suppressed by the COX-2 inhibitor NS-398. Forced expression of KIAA1199 increases low-molecular-weight HA in conditioned medium. siRNA knockdown decreases cell migration and proliferation in pancreatic cancer. siRNA knockdown, gene transduction (overexpression), IL-1β stimulation, NS-398 treatment, HA molecular weight analysis of conditioned medium Oncotarget Medium 28179576
2017 KIAA1199 interacts with WBP11 (WW domain binding protein 11) and PTP4A3 (protein tyrosine phosphatase type IVA, member 3). This binding activates FGFR4/Wnt/β-catenin and EGFR signaling pathways to regulate E-cadherin and N-cadherin expression. Ectopic expression of WBP11 or PTP4A3 blocked KIAA1199-stimulated cell proliferation and migration. Co-immunoprecipitation, overexpression/knockdown, Western blotting, in vitro and in vivo functional assays Oncogene Medium 30626935
2017 KIAA1199 promotes Nrg1-dependent MEK1 and ERK1/2 activation in Schwann cells. In the absence of KIAA1199, SC dedifferentiation is impaired: cJun and negative regulators of myelination are decreased while Krox20 is elevated, driving a pro-myelinating phenotype. KIAA1199-deficient SCs show lower myelin clearance and increased myelination capacity. RNA interference, conditional Cre-lox knockout mice (tamoxifen-inducible), Nrg1 stimulation, Western blotting for MEK/ERK pathway components, myelination assays Glia High 28699206
2018 CEMIP localizes to endosomes where it acts as a scaffold protein binding MEK1, sustaining ERK1/2 activation in BRAF-mutated MEK1-inhibitor-resistant colorectal cancers. CEMIP expression is induced by β-catenin- and FRA-1-dependent Wnt pathway activation. CEMIP-dependent ERK1/2 signaling maintains c-Myc protein levels, providing metabolic advantage to resistant cells. siRNA knockdown, co-immunoprecipitation (CEMIP–MEK1 interaction), endosomal fractionation, Western blotting, intestinal organoids, in vivo mouse models Cancer research High 29915160
2018 The AMPK/GSK3β/β-catenin cascade drives CEMIP overexpression in anoikis-resistant prostate cancer cells. CEMIP promotes migration, invasion, and metabolic reprogramming via PDK4 upregulation, increasing pyruvate and lactate production. CRISPR knockout of CEMIP reversed these effects and reduced MMP2, VEGF, PDK4, and lactate dehydrogenase A expression. CRISPR/Cas9 knockout, Western blotting, metabolic assays (pyruvate, lactate, ATP), genome microarray, migration/invasion assays FASEB journal Medium 29505302
2018 KIAA1199 interacts with protein phosphatase 2A (PP2A) through its C-terminal domain and increases PP2A phosphatase activity. Downstream, stathmin (a microtubule-destabilizing protein) is dephosphorylated, leading to microtubule destabilization and enhanced cell motility. Paclitaxel (microtubule-stabilizing drug) prevents KIAA1199-induced microtubule destabilization. Co-immunoprecipitation (KIAA1199-PP2A), phosphatase activity assays, stathmin phosphorylation Western blotting, microtubule polymerization assays, paclitaxel rescue, in vivo orthotopic model Oncogene High 30202098
2018 HYBID/KIAA1199 is indispensable for HA depolymerization in skin fibroblasts; TMEM2 knockdown unexpectedly enhanced HA depolymerization rather than reducing it, demonstrating that TMEM2 is not involved as a catalytic hyaluronidase in HYBID-mediated HA depolymerization. TGF-β1 coordinately suppresses HYBID expression and upregulates TMEM2 expression. siRNA knockdown of HYBID and TMEM2 separately, HA depolymerization assay, TGF-β1 and growth factor treatment, multiple cell lines Biochemical and biophysical research communications Medium 30241936
2018 CEMIP upregulates BiP transcript and protein levels by mediating activation of the BiP promoter in breast cancer cells. CEMIP overexpression confers protective adaptations to hypoxia (decreased apoptosis, activated autophagy, increased glucose uptake). BiP signals downstream of CEMIP to modulate cellular resistance to hypoxia; reducing BiP in CEMIP-expressing cells sensitized cells to hypoxia and caused tumor regression in vivo. BiP promoter reporter assay, siRNA knockdown, overexpression, hypoxia treatment, apoptosis/autophagy assays, glucose uptake assay, in vivo xenograft Oncotarget Medium 31303964
2019 CEMIP protein is elevated in exosomes from brain metastatic cancer cells. Uptake of CEMIP+ exosomes by brain endothelial and microglial cells induces endothelial cell branching and inflammation in the perivascular niche, upregulating pro-inflammatory cytokines (Ptgs2, Tnf, Ccl/Cxcl) that promote brain vascular remodeling. CEMIP depletion in tumor cells impaired brain metastasis and tumor-vasculature association, phenotypes rescued by pre-conditioning the brain with CEMIP+ exosomes. Proteomic analysis of exosomes, CEMIP depletion (genetic), exosome uptake experiments, brain endothelial/microglial co-culture, cytokine profiling, in vivo brain metastasis model with exosome pre-conditioning Nature cell biology High 31685984
2019 CEMIP promotes fibrosis-like transdifferentiation of OA chondrocytes into 'chondro-myo-fibroblasts' expressing α-SMA and type III collagen. CEMIP regulates β-catenin protein level, is required for chondrocyte proliferation, and promotes TGFβ signaling via the p-Smad2/3 (Alk5/PAI-1) pathway. CEMIP expression is induced by the pSmad1/5 (Alk1) pathway. siRNA knockdown, high-throughput RNA sequencing, Western blotting, in vitro chondrocyte dedifferentiation model, human and mouse OA tissue analysis, in situ co-localization Cell death & disease Medium 30718510
2019 KIAA1199 promotes osteoblastic stem cell (hMSC) migration. KIAA1199-deficient hMSCs show changes in cell morphology, reduced F-actin polymerization, and altered phosphorylation of cofilin1 (CFL1) and LIM-domain kinase 1 (LIMK1). KIAA1199 activates P38 kinase and its associated changes in Wnt signaling; impaired Wnt/TCF reporter activity in KIAA1199-deficient hMSCs was rescued by KIAA1199 treatment. shRNA knockdown, scratch assay, trans-well migration, F-actin staining, Western blotting (pCFL1, pLIMK1, DSTN), TCF-reporter assay, P38 kinase assay, rescue with recombinant KIAA1199 Cell death & disease Medium 30755597
2020 Cemip is the major inducible gene responsible for hyaluronan catabolism in mouse dermis upon S. aureus infection. Cemip-/- mice failed to digest hyaluronan and had significantly less infection after intradermal S. aureus challenge. Stabilization of large-MW HA in Cemip-/- mice enabled increased cathelicidin antimicrobial peptide (Camp) expression, partly through enhanced differentiation of preadipocytes to adipocytes. Cemip-/- mice also showed greater IL-6 expression and neutrophil infiltration. Cemip knockout mice (genetic), intradermal S. aureus challenge, HA molecular weight analysis, Camp/antimicrobial peptide expression, histology (Pref1, PPARγ, Adipoq markers), IL-6 and neutrophil quantification Cell reports High 31914398
2020 HYBID/KIAA1199 knockout mice show decreased dendritic spine density in the dentate gyrus granule cells, accompanied by HA accumulation and decreased doublecortin-positive immature neurons in the dentate gyrus, suggesting HYBID-mediated HA degradation is critical for synaptic formation and cognitive function. Hybid knockout mice, Golgi-Cox staining (dendritic spine density), HA staining, doublecortin immunostaining Biochemical and biophysical research communications Medium 30060951
2020 Histamine increases HA degradation in skin fibroblasts by up-regulating HYBID/KIAA1199 and down-regulating HAS2. The histamine H1 receptor mediates these effects. HYBID up-regulation requires protein kinase Cδ signaling, while HAS2 suppression requires PI3K-Akt signaling downstream of H1 receptor. Histamine H1 agonist/antagonist, PKCδ inhibitor, PI3K-Akt inhibitor, HA molecular weight analysis, HYBID/HAS2 expression analysis, immunohistochemistry in human skin biopsies The Journal of biological chemistry High 31949043
2021 Secreted KIAA1199 mediates extracellular HA degradation by attaching to the cell membrane of RA fibroblast-like synoviocytes via its G8 domain binding to ANXA1. In vivo, KIAA1199 knockout mice showed greater resistance to collagen-induced arthritis, partially reversed by intra-articular injection of full-length but not G8-deleted KIAA1199. NF-κB activation by IL-6 through PI3K/Akt signaling is the main pathway inducing KIAA1199 expression in RA FLS. Anti-KIAA1199 mAb treatment, KIAA1199 KO mice, collagen-induced arthritis model, intra-articular gene injection (WT vs G8-deleted mutant), cell membrane binding assay, HA degradation assay, NF-κB/PI3K/Akt inhibitor analysis Cell death & disease High 33473125
2021 CEMIP acts as a novel adaptor protein for O-GlcNAc transferase (OGT). CEMIP interacts with OGT and β-catenin, leading to elevated O-GlcNAcylation of β-catenin and enhanced β-catenin nuclear translocation. Nuclear β-catenin then enhances CEMIP transcription in a reciprocal positive feedback loop and upregulates glutaminase 1, SLC1A5, and SLC38A2 (glutamine transporters) to promote glutamine metabolic reprogramming and CRC metastasis. Co-immunoprecipitation (CEMIP-OGT-β-catenin complex), O-GlcNAcylation assay, β-catenin nuclear fractionation, transcriptional reporter, in vivo CRC metastasis model with combinational inhibition Oncogene High 34608265
2022 ATF4 triggers CEMIP transcription during ECM detachment, and elevated CEMIP promotes PKCα membrane translocation, leading to serine-70 phosphorylation of Bcl-2. This phosphorylation dissociates the Bcl-2/Beclin1 complex, inducing protective autophagy and anoikis resistance in prostate cancer cells. siRNA knockdown, Western blotting (pBcl-2 Ser70, Beclin1 complex), PKCα translocation assay, autophagy flux assay, ATF4 ChIP/promoter analysis, in vivo metastasis model Cell death & disease Medium 35013120
2022 CEMIP promotes ferroptosis resistance during ECM detachment by promoting cystine uptake. Mechanistically, CEMIP interacts with ITPR3 to modulate ER calcium leakage, activating CaMKII, which phosphorylates NRF2 and promotes its nuclear localization, leading to elevated SLC7A11 transcription (a cystine/glutamate antiporter). Silencing CEMIP abolishes cystine uptake promotion and ferroptosis resistance. Co-immunoprecipitation (CEMIP-ITPR3), CaMKII activity assay, NRF2 nuclear fractionation, SLC7A11 expression analysis, cystine uptake assay, ferroptosis assays, siRNA knockdown Cancer science Medium 35363929
2022 CEMIP acts as an adaptor for the interaction between MHC-I and clathrin, driving MHC-I internalization via clathrin-dependent endocytosis in colorectal cancer cells. Internalized MHC-I is anchored to lysosomes for degradation, disrupting MHC-I recycling to the cell surface and reducing CD8+ T cell cytotoxicity. Co-immunoprecipitation, proximity ligation assay (CEMIP–MHC-I–clathrin), immunofluorescence (intracellular MHC-I trafficking), flow cytometry (surface MHC-I), in vivo murine CRC model, CD8+ T cell cytotoxicity assay Journal for immunotherapy of cancer High 36596591
2022 KIAA1199 activates TGFβ signaling by interacting with TGFBR1/2, stimulating CXCL1 and CXCL3 production, driving aggregation of immunosuppressive neutrophils that facilitate CRC liver metastasis. Co-immunoprecipitation (KIAA1199-TGFBR1/2), flow cytometry (immune cell infiltration), CXCL1/3 ELISA, siRNA knockdown, in vivo mouse CRC metastasis model Hepatology (Baltimore, Md.) Medium 35108400
2022 HIF1α lactylation (by lactate imported via MCT1) stabilizes HIF1α under normoxia. Lactylated HIF1α is a transcriptional enhancer of KIAA1199, as shown by dual-luciferase and ChIP-PCR. KIAA1199 in turn promotes angiogenesis and vasculogenic mimicry by increasing secretory VEGFA and decreasing sema3A, while elevating depolymerized HA levels; the HA biosynthesis inhibitor 4MU reversed these effects. Dual-luciferase reporter, ChIP-PCR, VEGFA ELISA, sema3A/VEGFA Western blotting, tube formation assay, 4MU treatment, in vivo tumorigenesis International journal of biological macromolecules Medium 36209908
2023 KIAA1199 deficiency in bone marrow stromal cells (hMSCs) enhances osteoblast differentiation and increases bone mass in vivo. Mechanistically, KIAA1199 inhibits osteopontin production by osteoblasts via integrin-mediated AKT and ERK-MAPK intracellular signaling. KIAA1199 KO mice are protected from ovariectomy-induced bone loss and show accelerated healing of bone defects. KIAA1199 knockout mice, ectopic bone formation assay, in vitro osteoblast differentiation, Western blotting (AKT, ERK-MAPK), integrin inhibition, osteopontin expression analysis, micro-CT, biomechanical testing Nature communications High 37037828
2023 CEMIP acts as a scaffold protein bridging MIB1 (an E3 ubiquitin ligase) and GRAF1. CEMIP interacts with the SH3 domain of GRAF1 through its 295-819aa domain and negatively regulates GRAF1 stability by facilitating MIB1-mediated ubiquitination and degradation of GRAF1. GRAF1 degradation activates CDC42/MAPK pathway-regulated EMT, promoting CRC metastasis. Co-immunoprecipitation (CEMIP-GRAF1-MIB1), domain mapping (295-819aa), ubiquitination assay, CDC42 activity assay, Western blotting, in vivo CRC metastasis model, CDC42 inhibitor Cell death & disease High 36849460
2023 Human TMEM2 does not function as a catalytic hyaluronidase (in contrast to mouse TMEM2). In HEK293T cells, human HYBID and mouse TMEM2, but not human TMEM2, degraded extracellular HA. Chimeric domain analysis identified mouse GG domain residues His248 and Ala303 as critical for HA-degrading activity; replacing these with corresponding human TMEM2 residues (Asn248, Phe303) abolished mTMEM2 activity. In fibroblasts, hTMEM2 regulates HA metabolism by modulating HYBID and HAS2 expression. HEK293T transfection with human HYBID, mTMEM2, hTMEM2, and chimeric constructs; HA degradation assay; site-directed mutagenesis; siRNA knockdown of hTMEM2; HYBID/HAS2 expression analysis The Journal of biological chemistry High 37196767
2023 CEMIP inhibits c-Myc ubiquitination by hindering the interaction between FBXW7 (E3 ubiquitin ligase) and c-Myc, increasing c-Myc stabilization and nuclear accumulation, thereby promoting glutamine-dependent SCLC cell proliferation. LC-MS/MS proteomics, co-immunoprecipitation (CEMIP-FBXW7-c-Myc), ubiquitination assay, c-Myc nuclear fractionation, GLS1 inhibitor CB-839, in vivo/in vitro functional assays Biochemical pharmacology Medium 36746261
2024 ALKBH5 (m6A demethylase) negatively regulates CEMIP expression by reducing the stability of CEMIP mRNA. Reduced ALKBH5 in paclitaxel-resistant NSCLC cells leads to elevated CEMIP, promoting EMT and drug resistance; ALKBH5 overexpression reverses EMT and restores paclitaxel sensitivity. RNA-seq, RT-PCR, Western blotting, mRNA stability assay, ALKBH5 overexpression/knockdown, paclitaxel sensitivity assay, EMT marker analysis Toxicology and applied pharmacology Medium 38199493
2003 A point mutation H783Y in KIAA1199 causes an unusual cytoplasmic distribution pattern distinct from the localization of wild-type protein, suggesting altered subcellular trafficking as a potential mechanism of hearing impairment. Site-directed mutagenesis, in vitro subcellular localization by microscopy Journal of human genetics Low 14577002

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2019 Tumour exosomal CEMIP protein promotes cancer cell colonization in brain metastasis. Nature cell biology 347 31685984
2013 KIAA1199, a deafness gene of unknown function, is a new hyaluronan binding protein involved in hyaluronan depolymerization. Proceedings of the National Academy of Sciences of the United States of America 228 23509262
2022 HIF1α lactylation enhances KIAA1199 transcription to promote angiogenesis and vasculogenic mimicry in prostate cancer. International journal of biological macromolecules 210 36209908
2013 Unraveling the role of KIAA1199, a novel endoplasmic reticulum protein, in cancer cell migration. Journal of the National Cancer Institute 115 23990668
2003 Mutations in the gene encoding KIAA1199 protein, an inner-ear protein expressed in Deiters' cells and the fibrocytes, as the cause of nonsyndromic hearing loss. Journal of human genetics 113 14577002
2014 NF-κB-induced KIAA1199 promotes survival through EGFR signalling. Nature communications 102 25366117
2011 Repression of KIAA1199 attenuates Wnt-signalling and decreases the proliferation of colon cancer cells. British journal of cancer 95 21772334
2018 LncRNA TUG1 promoted KIAA1199 expression via miR-600 to accelerate cell metastasis and epithelial-mesenchymal transition in colorectal cancer. Journal of experimental & clinical cancer research : CR 85 29776371
2009 Clinicopathologic significance of KIAA1199 overexpression in human gastric cancer. Annals of surgical oncology 81 19434458
2017 Down-regulation of KIAA1199/CEMIP by miR-216a suppresses tumor invasion and metastasis in colorectal cancer. International journal of cancer 77 28213952
2015 Regulation of Hyaluronan (HA) Metabolism Mediated by HYBID (Hyaluronan-binding Protein Involved in HA Depolymerization, KIAA1199) and HA Synthases in Growth Factor-stimulated Fibroblasts. The Journal of biological chemistry 76 26518873
2018 AMPK/GSK3β/β-catenin cascade-triggered overexpression of CEMIP promotes migration and invasion in anoikis-resistant prostate cancer cells by enhancing metabolic reprogramming. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 75 29505302
2019 CEMIP (KIAA1199) induces a fibrosis-like process in osteoarthritic chondrocytes. Cell death & disease 72 30718510
2005 Upregulation of the KIAA1199 gene is associated with cellular mortality. Cancer letters 71 16157444
2022 ATF4/CEMIP/PKCα promotes anoikis resistance by enhancing protective autophagy in prostate cancer cells. Cell death & disease 66 35013120
2022 KIAA1199 drives immune suppression to promote colorectal cancer liver metastasis by modulating neutrophil infiltration. Hepatology (Baltimore, Md.) 64 35108400
2015 Induction of KIAA1199/CEMIP is associated with colon cancer phenotype and poor patient survival. Oncotarget 64 26437221
2014 Functional proteomic analysis reveals the involvement of KIAA1199 in breast cancer growth, motility and invasiveness. BMC cancer 64 24628760
2019 The miR-29c-KIAA1199 axis regulates gastric cancer migration by binding with WBP11 and PTP4A3. Oncogene 61 30626935
2019 KIAA1199 promotes sorafenib tolerance and the metastasis of hepatocellular carcinoma by activating the EGF/EGFR-dependent epithelial-mesenchymal transition program. Cancer letters 57 30980868
2015 Hypoxia promotes colon cancer dissemination through up-regulation of cell migration-inducing protein (CEMIP). Oncotarget 57 26009875
2019 Functional role of long non-coding RNA CASC19/miR-140-5p/CEMIP axis in colorectal cancer progression in vitro. World journal of gastroenterology 56 31011255
2013 Early insights into the function of KIAA1199, a markedly overexpressed protein in human colorectal tumors. PloS one 53 23936024
2017 Silencing of CEMIP suppresses Wnt/β-catenin/Snail signaling transduction and inhibits EMT program of colorectal cancer cells. Acta histochemica 52 29173982
2021 CEMIP, a novel adaptor protein of OGT, promotes colorectal cancer metastasis through glutamine metabolic reprogramming via reciprocal regulation of β-catenin. Oncogene 47 34608265
2016 Crohn's Disease Fibroblasts Overproduce the Novel Protein KIAA1199 to Create Proinflammatory Hyaluronan Fragments. Cellular and molecular gastroenterology and hepatology 47 27981209
2014 KIAA1199 and its biological role in human cancer and cancer cells (review). Oncology reports 47 24573670
2018 KIAA1199 promotes invasion and migration in non-small-cell lung cancer (NSCLC) via PI3K-Akt mediated EMT. Journal of molecular medicine (Berlin, Germany) 45 30478628
2019 CEMIP promotes ovarian cancer development and progression via the PI3K/AKT signaling pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 44 30925458
2014 KIAA1199 interacts with glycogen phosphorylase kinase β-subunit (PHKB) to promote glycogen breakdown and cancer cell survival. Oncotarget 44 25051373
2019 Long non‑coding RNA HCP5 promotes prostate cancer cell proliferation by acting as the sponge of miR‑4656 to modulate CEMIP expression. Oncology reports 43 31746434
2013 N-Terminal signal sequence is required for cellular trafficking and hyaluronan-depolymerization of KIAA1199. FEBS letters 42 24269685
2017 Distribution and function of hyaluronan binding protein involved in hyaluronan depolymerization (HYBID, KIAA1199) in the mouse central nervous system. Neuroscience 41 28189611
2018 KIAA1199 promotes metastasis of colorectal cancer cells via microtubule destabilization regulated by a PP2A/stathmin pathway. Oncogene 40 30202098
2013 Murine homologue of the human KIAA1199 is implicated in hyaluronan binding and depolymerization. FEBS open bio 40 24251095
2022 CEMIP promotes extracellular matrix-detached prostate cancer cell survival by inhibiting ferroptosis. Cancer science 39 35363929
2018 The role and regulation of TMEM2 (transmembrane protein 2) in HYBID (hyaluronan (HA)-binding protein involved in HA depolymerization/ KIAA1199/CEMIP)-mediated HA depolymerization in human skin fibroblasts. Biochemical and biophysical research communications 39 30241936
2020 Hyaluronan Degradation by Cemip Regulates Host Defense against Staphylococcus aureus Skin Infection. Cell reports 38 31914398
2020 circ_001653 Silencing Promotes the Proliferation and ECM Synthesis of NPCs in IDD by Downregulating miR-486-3p-Mediated CEMIP. Molecular therapy. Nucleic acids 38 32203911
2018 Reduction of hyaluronan and increased expression of HYBID (alias CEMIP and KIAA1199) correlate with clinical symptoms in photoaged skin. The British journal of dermatology 38 29330857
2018 The Endosomal Protein CEMIP Links WNT Signaling to MEK1-ERK1/2 Activation in Selumetinib-Resistant Intestinal Organoids. Cancer research 38 29915160
2017 Central Role of CEMIP in Tumorigenesis and Its Potential as Therapeutic Target. Journal of Cancer 38 28819426
2017 KIAA1199 is induced by inflammation and enhances malignant phenotype in pancreatic cancer. Oncotarget 37 28179576
2023 Tumor CEMIP drives immune evasion of colorectal cancer via MHC-I internalization and degradation. Journal for immunotherapy of cancer 36 36596591
2019 KIAA1199 is a secreted molecule that enhances osteoblastic stem cell migration and recruitment. Cell death & disease 36 30755597
2021 Secreted KIAA1199 promotes the progression of rheumatoid arthritis by mediating hyaluronic acid degradation in an ANXA1-dependent manner. Cell death & disease 35 33473125
2020 Implication of HYBID (Hyaluronan-Binding Protein Involved in Hyaluronan Depolymerization) in Hyaluronan Degradation by Synovial Fibroblasts in Patients with Knee Osteoarthritis. The American journal of pathology 34 32084364
2021 Decreased expression of ATF3, orchestrated by β-catenin/TCF3, miR-17-5p and HOXA11-AS, promoted gastric cancer progression via increased β-catenin and CEMIP. Experimental & molecular medicine 32 34728784
2021 The emerging role of KIAA1199 in cancer development and therapy. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 31 33773462
2019 Role of HYBID (Hyaluronan Binding Protein Involved in Hyaluronan Depolymerization), Alias KIAA1199/CEMIP, in Hyaluronan Degradation in Normal and Photoaged Skin. International journal of molecular sciences 31 31752258
2018 Combined use of CEMIP and CA 19-9 enhances diagnostic accuracy for pancreatic cancer. Scientific reports 31 29467409
2015 KIAA1199 as a potential diagnostic biomarker of rheumatoid arthritis related to angiogenesis. Arthritis research & therapy 31 26022278
2023 KIAA1199 deficiency enhances skeletal stem cell differentiation to osteoblasts and promotes bone regeneration. Nature communications 30 37037828
2019 CEMIP upregulates BiP to promote breast cancer cell survival in hypoxia. Oncotarget 30 31303964
2018 Targeted deletion of HYBID (hyaluronan binding protein involved in hyaluronan depolymerization/ KIAA1199/CEMIP) decreases dendritic spine density in the dentate gyrus through hyaluronan accumulation. Biochemical and biophysical research communications 30 30060951
2022 CEMIP (KIAA1199) regulates inflammation, hyperplasia and fibrosis in osteoarthritis synovial membrane. Cellular and molecular life sciences : CMLS 29 35474501
2022 CEMIP, a Promising Biomarker That Promotes the Progression and Metastasis of Colorectal and Other Types of Cancer. Cancers 29 36291875
2019 KIAA1199, a Target of MicoRNA-486-5p, Promotes Papillary Thyroid Cancer Invasion by Influencing Epithelial-Mesenchymal Transition (EMT). Medical science monitor : international medical journal of experimental and clinical research 28 31501407
2022 CEMIP (HYBID, KIAA1199): structure, function and expression in health and disease. The FEBS journal 26 35997767
2008 The localization of proteins encoded by CRYM, KIAA1199, UBA52, COL9A3, and COL9A1, genes highly expressed in the cochlea. Neuroscience 24 18448257
2023 Inhibition of CEMIP potentiates the effect of sorafenib on metastatic hepatocellular carcinoma by reducing the stiffness of lung metastases. Cell death & disease 23 36639658
2020 CEMIP regulates the proliferation and migration of vascular smooth muscle cells in atherosclerosis through the WNT-beta-catenin signaling pathway. Biochemistry and cell biology = Biochimie et biologie cellulaire 23 32207314
2020 Induction of CEMIP in Chondrocytes by Inflammatory Cytokines: Underlying Mechanisms and Potential Involvement in Osteoarthritis. International journal of molecular sciences 23 32365591
2020 Downregulation of KIAA1199 by miR-486-5p suppresses tumorigenesis in lung cancer. Cancer medicine 23 32519472
2016 Identification of KIAA1199 as a Biomarker for Pancreatic Intraepithelial Neoplasia. Scientific reports 22 27922049
2023 Human TMEM2 is not a catalytic hyaluronidase, but a regulator of hyaluronan metabolism via HYBID (KIAA1199/CEMIP) and HAS2 expression. The Journal of biological chemistry 21 37196767
2020 A novel metastatic promoter CEMIP and its downstream molecular targets and signaling pathway of cellular migration and invasion in SCLC cells based on proteome analysis. Journal of cancer research and clinical oncology 21 32648226
2017 Knockdown of CEMIP suppresses proliferation and induces apoptosis in colorectal cancer cells: downregulation of GRP78 and attenuation of unfolded protein response. Biochemistry and cell biology = Biochimie et biologie cellulaire 21 29024602
2022 Loss of REST in breast cancer promotes tumor progression through estrogen sensitization, MMP24 and CEMIP overexpression. BMC cancer 20 35177031
2022 CEMIP Promotes Osteosarcoma Progression and Metastasis Through Activating Notch Signaling Pathway. Frontiers in oncology 20 35957875
2021 The role of CEMIP in tumors: An update based on cellular and molecular insights. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 20 34922110
2020 Cell migration inducing hyaluronidase 1 (CEMIP) activates STAT3 pathway to facilitate cell proliferation and migration in breast cancer. Journal of receptor and signal transduction research 20 32757700
2018 miR-140-5p suppresses retinoblastoma cell proliferation, migration, and invasion by targeting CEMIP and CADM3. Cellular and molecular biology (Noisy-le-Grand, France) 20 29808799
2023 CEMIP promotes small cell lung cancer proliferation by activation of glutamine metabolism via FBXW7/c-Myc-dependent axis. Biochemical pharmacology 18 36746261
2023 BMP6 knockdown enhances cardiac fibrosis in a mouse myocardial infarction model by upregulating AP-1/CEMIP expression. Clinical and translational medicine 18 37313693
2021 MiR-148a-3p targets CEMIP to suppress the genesis of gastric cancer cells. Biochemical and biophysical research communications 18 34455220
2020 HYBID (alias KIAA1199/CEMIP) and hyaluronan synthase coordinately regulate hyaluronan metabolism in histamine-stimulated skin fibroblasts. The Journal of biological chemistry 18 31949043
2019 Inhibitory effects of Sanguisorba officinalis root extract on HYBID (KIAA1199)-mediated hyaluronan degradation and skin wrinkling. International journal of cosmetic science 18 30485450
2019 Knockdown of KIAA1199 suppresses IL-1β-induced cartilage degradation and inflammatory responses in human chondrocytes through the Wnt/β-catenin signalling pathway. International immunopharmacology 18 31103876
2018 Knockdown of KIAA1199 attenuates growth and metastasis of hepatocellular carcinoma. Cell death discovery 18 30455988
2023 CEMIP, acting as a scaffold protein for bridging GRAF1 and MIB1, promotes colorectal cancer metastasis via activating CDC42/MAPK pathway. Cell death & disease 17 36849460
2021 Pro-inflammatory cytokines suppress HYBID (hyaluronan (HA) -binding protein involved in HA depolymerization/KIAA1199/CEMIP) -mediated HA metabolism in human skin fibroblasts. Biochemical and biophysical research communications 15 33422943
2021 LncRNA LINC00958 promotes tumor progression through miR-4306/CEMIP axis in osteosarcoma. European review for medical and pharmacological sciences 15 33928604
2021 miR-4677-3p participates proliferation and metastases of gastric cancer cell via CEMIP-PI3K/AKT signaling pathway. Cell cycle (Georgetown, Tex.) 15 34437815
2021 Hypoxia increases KIAA1199/CEMIP expression and enhances cell migration in pancreatic cancer. Scientific reports 15 34521918
2016 Distinct Expression Pattern of a Deafness Gene, KIAA1199, in a Primate Cochlea. BioMed research international 15 27403418
2021 The Attenuated Secretion of Hyaluronan by UVA-Exposed Human Fibroblasts Is Associated with Up- and Downregulation of HYBID and HAS2 Expression via Activated and Inactivated Signaling of the p38/ATF2 and JAK2/STAT3 Cascades. International journal of molecular sciences 14 33669634
2021 Deletion of Hyaluronan-Binding Protein Involved in Hyaluronan Depolymerization (HYBID) Results in Attenuation of Osteoarthritis in Mice. The American journal of pathology 14 34390681
2018 Relationship of hyaluronan and HYBID (KIAA1199) expression with roughness parameters of photoaged skin in Caucasian women. Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) 14 29536579
2018 KIAA1199 expression and hyaluronan degradation colocalize in multiple sclerosis lesions. Glycobiology 14 30007349
2017 KIAA1199: A novel regulator of MEK/ERK-induced Schwann cell dedifferentiation. Glia 14 28699206
2023 KIAA1199 promotes oxaliplatin resistance and epithelial mesenchymal transition of colorectal cancer via protein O-GlcNAcylation. Translational oncology 13 36610242
2022 CEMIP as a potential biomarker and therapeutic target for breast cancer patients. International journal of medical sciences 13 35370456
2022 Expression and regulation of recently discovered hyaluronidases, HYBID and TMEM2, in chondrocytes from knee osteoarthritic cartilage. Scientific reports 13 36241903
2022 circ-BPTF serves as a miR-486-5p sponge to regulate CEMIP and promotes hypoxic pulmonary arterial smooth muscle cell proliferation in COPD. Acta biochimica et biophysica Sinica 13 36514216
2021 HYBID derived from tumor cells and tumor-associated macrophages contribute to the glioblastoma growth. Brain research 12 33887254
2019 Clinical Significance of KIAA1199 as a Novel Target for Gastric Cancer Drug Therapy. Anticancer research 11 31810922
2024 ALKBH5 regulates paclitaxel resistance in NSCLC via inhibiting CEMIP-mediated EMT. Toxicology and applied pharmacology 10 38199493
2021 Therapeutic DNA vaccine encoding CEMIP (KIAA1199) ameliorates kidney fibrosis in obesity through inhibiting the Wnt/β-catenin pathway. Biochimica et biophysica acta. General subjects 10 34582938
2025 The crucial role of CEMIP in cancer metastasis: Mechanistic insights and clinical implications. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 9 39758005

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