Affinage

SOCS5

Suppressor of cytokine signaling 5 · UniProt O75159

Length
536 aa
Mass
61.2 kDa
Annotated
2026-06-10
65 papers in source corpus 18 papers cited in narrative 18 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

SOCS5 is an intracellular negative regulator of cytokine and growth-factor signaling that acts on the JAK-STAT and EGFR pathways through multiple, structurally distinct interaction modules (PMID:23990909, PMID:15695332). Its conserved N-terminal JAK interaction region (JIR), an intrinsically disordered segment containing a preformed α-helix (residues 224–233) whose JAK binding is modulated by Ser211 phosphorylation, directly binds the JAK kinase domain and selectively suppresses JAK1 and JAK2 (but not JAK3 or TYK2) autophosphorylation by a mechanism distinct from SOCS1/SOCS3; its SH2 domain additionally engages phosphoTyr317 of the adaptor Shc-1 (PMID:23990909, PMID:26173083). SOCS5 also binds the IL-4Rα cytoplasmic tail independently of receptor phosphorylation, displacing JAK1 from the receptor and inhibiting IL-4-driven STAT6 activation (PMID:12242343), and associates with the EGF receptor complex EGF-independently to inhibit mitogenic signaling, an effect that requires the SOCS box and is consistent with SOCS box-mediated recruitment of E3 ubiquitin ligase activity promoting EGFR degradation (PMID:15695332). Through this control of EGFR signaling SOCS5 restricts influenza A virus replication in airway epithelium, where its loss heightens disease severity and viral titres (PMID:28195529). SOCS5 is positioned as an inducible feedback node: it is transcriptionally upregulated by tyrosine-phosphorylated STAT3 binding SOCS promoter elements (PMID:17464217, PMID:27317770), translationally repressed by miR-124 (downstream of MeCP2) and other miRNAs (PMID:24619648), and epigenetically silenced by DNMT3A/MeCP2 in T-ALL, where silencing reactivates JAK-STAT signaling and accelerates leukemia progression (PMID:30974024). In hepatocellular carcinoma SOCS5 acquires oncogenic, signaling-independent functions: its SH2 domain (critical residues Y413/D443) binds the RBMX RRM domain, and the SOCS5-RBMX complex co-activates the SREBP1 promoter to drive de novo lipogenesis and metastasis (PMID:38429411), while SOCS5 also promotes HCC migration and invasion via PI3K/Akt/mTOR-mediated autophagy and a downstream HIF-1α axis (PMID:31406106, PMID:36319626). A Socs5 knockout shows the protein is dispensable for lymphocyte development and Th1/Th2 differentiation under standard conditions (PMID:15199163).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2000 Low

    Established SOCS5 as a candidate negative regulator of JAK signaling by cloning it and recognizing the SH2-domain/SOCS-box architecture that defines the SOCS family.

    Evidence cDNA cloning, Northern blot, and FISH chromosomal mapping

    PMID:10773671

    Open questions at the time
    • Function inferred from structural homology with no direct functional assay
    • No binding partner or substrate identified
    • Dual chromosomal mapping (2p21 and 3p22) unresolved
  2. 2002 High

    Provided the first mechanism, showing SOCS5 binds the IL-4Rα cytoplasmic tail independent of receptor phosphorylation to displace JAK1 and block STAT6, dampening Th2 differentiation.

    Evidence Co-IP, transgenic mouse overexpression, and Th2 differentiation assays

    PMID:12242343

    Open questions at the time
    • Phosphorylation-independent binding interface on IL-4Rα not mapped
    • Th2 role contradicted by later knockout data
    • Did not establish whether endogenous SOCS5 levels recapitulate the overexpression phenotype
  3. 2004 High

    Tested SOCS5 necessity genetically and found it dispensable for lymphocyte function and Th1/Th2 differentiation, narrowing where SOCS5 is physiologically required.

    Evidence Targeted gene-disruption knockout mouse with lymphocyte proliferation, Th1/Th2, and Leishmania infection readouts

    PMID:15199163

    Open questions at the time
    • Possible redundancy with other SOCS proteins not excluded
    • Conditions tested may not engage SOCS5-dependent contexts
    • Conflicts with the overexpression-based Th2 phenotype
  4. 2005 High

    Extended SOCS5 action to growth-factor signaling by showing EGF-independent association with the EGFR complex and SOCS-box-dependent inhibition of mitogenic signaling.

    Evidence Co-IP, SOCS-box deletion mutants, and proliferation assays in engineered EGF-responsive lines

    PMID:15695332

    Open questions at the time
    • E3 ligase recruitment and EGFR ubiquitination inferred but not directly demonstrated
    • Specific EGFR residues or adaptor mediating binding not defined
  5. 2013 High

    Defined the direct enzymatic mechanism, identifying the N-terminal JIR that binds the JAK kinase domain and selectively inhibits JAK1/JAK2 activity, plus an SH2-Shc-1 pY317 interaction.

    Evidence Co-expression autophosphorylation assays, in vitro kinase assays, domain mutagenesis, and SH2 binding assays

    PMID:23990909

    Open questions at the time
    • Structural basis of JAK1/JAK2 selectivity over JAK3/TYK2 unresolved
    • Functional consequence of Shc-1 pY317 binding in cells not established
  6. 2015 High

    Resolved the conformational basis of JAK recognition, showing the disordered JIR contains a preformed α-helix and a Ser211 phosphosite that tunes JAK binding.

    Evidence NMR chemical shift, relaxation, and NOE analysis with site-directed mutagenesis

    PMID:26173083

    Open questions at the time
    • Kinase responsible for Ser211 phosphorylation unknown
    • No co-structure of the JIR bound to JAK
  7. 2007 Medium

    Identified an upstream input, showing PMA-induced STAT3 binds SOCS promoter elements to drive SOCS5 transcription, placing SOCS5 in a feedback loop.

    Evidence Western blot for SOCS5, phospho-Stat3 detection, and EMSA in rat astrocytes

    PMID:17464217

    Open questions at the time
    • EMSA used generic SOCS promoter elements rather than dissecting the SOCS5 promoter specifically
    • Direct STAT3 occupancy of the SOCS5 locus not shown
  8. 2014 Medium

    Established post-transcriptional and epigenetic control, showing the MeCP2→miR-124 axis represses SOCS5 translation, with SOCS5 accumulation inhibiting STAT1/STAT3 and Th1/Th17 differentiation.

    Evidence MeCP2 knockdown/knockout in CD4+ T cells, miR-124 analysis, and Th1/Th17 differentiation assays

    PMID:24619648

    Open questions at the time
    • Direct miR-124 binding to the SOCS5 3'UTR not separately validated here
    • Mechanism of SOCS5-mediated STAT1/STAT3 inhibition in this context not dissected
  9. 2016 Medium

    Linked SOCS5 regulation to immune dysfunction, showing IL-10/STAT3-driven SOCS5 upregulation blocks STAT6 and impairs dendritic cell maturation in CLL, and miR-432 loss raises SOCS5 to suppress STAT1 antiviral signaling during JEV infection.

    Evidence Patient-derived cells with IL-10 mimicry and DC differentiation assays (CLL); 3'UTR luciferase reporter, siRNA rescue, and ISRE/viral replication assays (JEV)

    PMID:27282499 PMID:27317770

    Open questions at the time
    • Whether SOCS5-mediated STAT inhibition uses JAK displacement or kinase inhibition in these settings not resolved
    • Direct SOCS5 occupancy of receptors in patient cells not shown
  10. 2017 High

    Demonstrated a physiological antiviral role, showing SOCS5 restricts influenza A in airway epithelium via EGFR regulation, with loss worsening disease and restoration protecting COPD epithelium.

    Evidence Socs5 knockout mice, viral titration, weight loss, and restoration in primary epithelial cells

    PMID:28195529

    Open questions at the time
    • Molecular link between SOCS5-EGFR control and viral restriction not fully detailed
    • Relevance of JAK-inhibitory function to this phenotype not separated from EGFR function
  11. 2018 Medium

    Assigned SOCS5 a tumor-suppressor role in liver cancer through TSC1/mTOR regulation, with miR-18a and miR-25 directly targeting SOCS5 to drive HCC.

    Evidence miRNA luciferase target validation, SOCS5 gain/loss-of-function, and TSC1/mTOR Western blots

    PMID:30191950

    Open questions at the time
    • Conflicts with reports of oncogenic SOCS5 function in HCC
    • Mechanistic link between SOCS5 and TSC1 not biochemically defined
  12. 2019 Medium

    Revealed context-dependent oncogenic activity, showing SOCS5 promotes HCC migration/invasion via PI3K/Akt/mTOR-mediated autophagy, and that DNMT3A/MeCP2-driven SOCS5 silencing accelerates T-ALL by reactivating JAK-STAT.

    Evidence SOCS5 knockdown/overexpression with pathway Western blots and in vivo metastasis (HCC); epigenetic inhibition and xenograft (T-ALL)

    PMID:30974024 PMID:31406106

    Open questions at the time
    • Opposing tumor-suppressor vs oncogenic roles of SOCS5 in HCC unreconciled
    • Direct molecular target linking SOCS5 to PI3K/Akt/mTOR not identified
  13. 2022 Medium

    Expanded the HCC oncogenic mechanism through a HIF-1α axis and proposed a glioblastoma chemoresistance role via Bcl-2-mediated autophagy.

    Evidence SOCS5 knockdown with PI3K/mTOR inhibitor rescue and metastasis models (HCC); SOCS5 knockdown/overexpression with Bcl-2 rescue (GBM)

    PMID:35730472 PMID:36319626

    Open questions at the time
    • Bcl-2 transcriptional enhancement by SOCS5 lacks a direct promoter assay
    • How a SOCS-family signaling inhibitor mechanistically activates oncogenic axes remains undefined
  14. 2024 High

    Defined a non-canonical SOCS5 function, showing its SH2 domain (Y413/D443) binds the RBMX RRM domain and the complex co-activates the SREBP1 promoter to drive lipogenesis and HCC metastasis.

    Evidence Co-IP, GST-pulldown, SH2 point mutagenesis, SREBP1 promoter assay, proteomics, and metabolomics

    PMID:38429411

    Open questions at the time
    • How the SOCS5-RBMX complex engages the SREBP1 promoter mechanistically not resolved
    • Relationship of this nuclear/lipogenic role to SOCS5's cytoplasmic signaling-inhibitory functions unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SOCS5 switches between its canonical signaling-suppressor role (JAK inhibition, IL-4Rα/EGFR regulation) and its context-dependent oncogenic functions (RBMX/SREBP1 lipogenesis, PI3K/mTOR/HIF-1α) remains unresolved.
  • No structural model of full-length SOCS5 bound to JAK or EGFR
  • E3 ligase identity and direct ubiquitination substrates not confirmed
  • Opposing tumor-suppressor and oncogenic roles, especially in HCC, not reconciled

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0060090 molecular adaptor activity 2 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005829 cytosol 3
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-392499 Metabolism of proteins 1
Partners
EGFRIL4RJAK1JAK2RBMXSHC1

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 SOCS5 protein interacts with the cytoplasmic region of the IL-4Rα chain irrespective of receptor tyrosine phosphorylation, and this interaction reduces the association of JAK1 with the IL-4 receptor, resulting in inhibition of IL-4-mediated STAT6 activation and suppression of Th2 differentiation. Co-immunoprecipitation, transgenic mouse overexpression, Th2 differentiation assays Proceedings of the National Academy of Sciences of the United States of America High 12242343
2005 SOCS5 associates with the EGF receptor complex in an EGF-independent manner and inhibits EGF-driven mitogenic signaling; deletion of the SOCS5 SOCS box abolishes this inhibition, suggesting the mechanism involves SOCS box-mediated recruitment of E3 ubiquitin ligase activity leading to enhanced proteasomal degradation of the EGF-R. Co-immunoprecipitation, cell proliferation assay with SOCS5 mutants (SOCS box deletion), engineered EGF-responsive cell lines Proceedings of the National Academy of Sciences of the United States of America High 15695332
2004 Socs5-deficient mice generated by targeted gene disruption show no abnormalities in lymphocyte compartment, no deviations in antigen- or cytokine-induced B and T cell proliferation, and no defects in Th1/Th2 differentiation or resistance to Leishmania major infection, indicating SOCS5 is dispensable for regulation of lymphocyte function under these conditions. Targeted gene disruption (knockout mouse), lymphocyte proliferation assays, Th1/Th2 differentiation assays, Leishmania infection model Molecular and cellular biology High 15199163
2013 SOCS5 contains a conserved JAK interaction region (JIR) in its N-terminus that mediates direct binding to the JAK kinase domain; co-expression of SOCS5 specifically reduces JAK1 and JAK2 (but not JAK3 or TYK2) autophosphorylation via a mechanism requiring both the JIR and additional N-terminal sequences; SOCS5 can directly inhibit JAK1 kinase activity through a mechanism distinct from SOCS1/SOCS3; additionally, the SOCS5 SH2 domain binds phosphoTyr317 of the adaptor protein Shc-1 with high affinity. Co-expression autophosphorylation assays, in vitro kinase assays, domain deletion and mutagenesis, SH2 domain binding assays PloS one High 23990909
2015 NMR structural characterization of the JAK interaction region (JIR) within the intrinsically disordered N-terminus of SOCS5 reveals preformed structural elements including an α-helix (residues 224–233) preceded by a turn and extended structure; a phosphorylation site (Ser211) within the JIR was identified and site-directed mutagenesis showed phosphorylation modulates JAK binding. NMR (chemical shift analysis, relaxation measurements, NOE analysis), site-directed mutagenesis Biochemistry High 26173083
2017 SOCS5 restricts influenza A virus replication in airway epithelium through regulation of EGFR signaling; Socs5-deficient mice exhibit heightened disease severity with increased viral titres; restoration of SOCS5 levels in primary COPD epithelial cells (which have reduced SOCS5) restricted influenza infection. Socs5 knockout mice, viral titration, restoration experiments in primary epithelial cells, weight loss measurements eLife High 28195529
2016 In CLL patients, elevated SOCS5 (induced via IL-10-driven STAT3 activation) inhibits STAT6 activation downstream of IL-4Rα, thereby impairing differentiation of functionally mature dendritic cells; IL-10 treatment of healthy donor monocytes mimics this effect through STAT3-dependent SOCS5 upregulation. Western blot for signaling molecules, monocyte-derived DC differentiation assay, IL-10 treatment, flow cytometry for DC surface markers and cytokine secretion Oncotarget Medium 27317770
2014 MeCP2 promotes expression of miR-124, which represses translation of SOCS5 mRNA; loss of MeCP2 leads to SOCS5 accumulation, which in turn inhibits cytokine-dependent activation of STAT1 and STAT3, impairing Th1 and Th17 cell differentiation. MeCP2 knockdown/knockout in CD4+ T cells, miR-124 expression analysis, Western blot for SOCS5 and phospho-STAT1/STAT3, Th1/Th17 differentiation assays Science signaling Medium 24619648
2016 JEV infection downregulates miR-432 in human brain microglial cells, causing upregulation of SOCS5; elevated SOCS5 suppresses STAT1 phosphorylation and ISRE activity, thereby dampening antiviral JAK-STAT signaling and promoting JEV replication; SOCS5 knockdown restored STAT1 phosphorylation and suppressed viral replication. 3'UTR luciferase reporter assay validating miR-432 targeting of SOCS5, miR-432 mimic/SOCS5 siRNA knockdown, Western blot for phospho-STAT1, ISRE reporter assay, viral replication assay Scientific reports Medium 27282499
2019 SOCS5 promotes HCC cell migration and invasion by inactivating PI3K/Akt/mTOR-mediated autophagy; dual inhibition of SOCS5 and mTOR further enhances autophagy and anti-metastatic effects; stable knockdown of SOCS5 reduces HCC cell metastasis in vivo. SOCS5 siRNA knockdown and overexpression, PI3K/Akt/mTOR pathway Western blot, autophagy assays, in vitro migration/invasion assays, in vivo metastasis model Cell death & disease Medium 31406106
2018 SOCS5 acts as a tumor suppressor in liver cancer by regulating TSC1 and downstream mTOR signaling; miR-18a and miR-25 directly target SOCS5 to promote HCC tumorigenesis. miRNA target validation (luciferase reporter), SOCS5 overexpression/knockdown in HCC cell lines, Western blot for TSC1 and mTOR pathway components, cell proliferation assays International journal of cancer Medium 30191950
2019 SOCS5 expression in T-ALL is epigenetically silenced by DNMT3A-mediated DNA methylation and MeCP2-mediated histone deacetylation; SOCS5 silencing activates JAK-STAT signaling and accelerates T-ALL engraftment and leukemia progression in a xenograft model; SOCS5 negatively regulates IL-7 and IL-4 receptor signaling in T-ALL cells. DNMT3A/MeCP2 inhibition, SOCS5 overexpression/knockdown, Western blot for JAK-STAT pathway, cell cycle analysis, human T-ALL murine xenograft model Cancer science Medium 30974024
2024 SOCS5 interacts with RBMX via its SH2 domain (critical residues Y413 and D443 binding the RBMX RRM domain); the SOCS5-RBMX complex co-stimulates the SREBP1 promoter to induce de novo lipogenesis, promoting HCC metastasis; SH2 domain mutations Y413 and D443 abolish RBMX binding and reverse lipogenesis induction. Co-IP and GST-pulldown identifying SOCS5-RBMX interaction, SH2 domain point mutagenesis (Y413, D443), SREBP1 promoter assay, proteomics, metabolomics, in vitro and in vivo experiments NPJ precision oncology High 38429411
2007 PMA treatment of rat brain astrocytes induces SOCS5 protein expression via activation of Stat3 (tyrosine-phosphorylated Stat3 binds SOCS promoter elements), identifying Stat3-driven transcriptional induction as a mechanism for SOCS5 upregulation. Western blot for SOCS5 protein, phospho-Stat3 detection, gel-shift (EMSA) assay showing Stat3 binding to SOCS promoter elements Molecules and cells Medium 17464217
2022 SOCS5 knockdown inhibits HCC cell invasion and migration by suppressing HIF-1α expression, preventing HIF-1α-dependent mitochondrial damage; this effect operates through the PI3K/Akt/mTOR/HIF-1α signaling axis as confirmed by rescue experiments with PI3K and mTOR inhibitors. SOCS5 siRNA knockdown, CoCl2 hypoxia model, immunofluorescence, electron microscopy, PI3K/mTOR inhibitor rescue experiments, in vivo metastasis and xenograft models Cell death & disease Medium 36319626
2022 SOCS5 contributes to TMZ resistance in glioblastoma by enhancing Bcl-2 transcription, which promotes autophagy; knockdown of SOCS5 inhibits TMZ chemoresistance through inhibition of Bcl-2-mediated autophagy, and upregulation of Bcl-2 reverses this effect. SOCS5 knockdown/overexpression, Western blot for Bcl-2, autophagy assays, TMZ resistance assays, rescue experiments with Bcl-2 overexpression Bioengineered Low 35730472
2023 POU2F1 acts as an upstream transcriptional activator of SOCS5, and elevated SOCS5 promotes diabetic retinopathy progression by upregulating CDKN1A (p21), driving cell cycle arrest and cellular senescence; SOCS5 knockdown mitigated retinal tissue damage, vascular leakage, and DNA damage in DR models. siRNA silencing of POU2F1 and SOCS5, Western blot for CDKN1A, in vitro (HG-induced HRMECs) and in vivo (STZ-induced DR mouse) models, apoptosis and senescence assays Cell death discovery Low 41922309
2000 CIS6/SOCS5 was cloned as a human homologue with structural features (SH2 domain and SOCS box) consistent with the SOCS family of negative regulators of JAK signaling; its gene was mapped to human chromosome bands 2p21 and 3p22. cDNA cloning, Northern blot for tissue expression, fluorescence in situ hybridization for chromosomal mapping Cytogenetics and cell genetics Low 10773671

Source papers

Stage 0 corpus · 65 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Expression of the suppressor of cytokine signaling-5 (SOCS5) negatively regulates IL-4-dependent STAT6 activation and Th2 differentiation. Proceedings of the National Academy of Sciences of the United States of America 171 12242343
2019 SOCS5 inhibition induces autophagy to impair metastasis in hepatocellular carcinoma cells via the PI3K/Akt/mTOR pathway. Cell death & disease 111 31406106
2005 The control of allergic conjunctivitis by suppressor of cytokine signaling (SOCS)3 and SOCS5 in a murine model. Journal of immunology (Baltimore, Md. : 1950) 90 16210657
2005 Suppressor of cytokine signaling (SOCS)-5 is a potential negative regulator of epidermal growth factor signaling. Proceedings of the National Academy of Sciences of the United States of America 79 15695332
2017 Suppressor of cytokine signaling (SOCS)5 ameliorates influenza infection via inhibition of EGFR signaling. eLife 65 28195529
2016 Japanese Encephalitis Virus exploits the microRNA-432 to regulate the expression of Suppressor of Cytokine Signaling (SOCS) 5. Scientific reports 64 27282499
2004 SOCS5 is expressed in primary B and T lymphoid cells but is dispensable for lymphocyte production and function. Molecular and cellular biology 58 15199163
2020 MicroRNA-301a promotes pancreatic cancer invasion and metastasis through the JAK/STAT3 signaling pathway by targeting SOCS5. Carcinogenesis 53 31233116
2014 MeCP2 reinforces STAT3 signaling and the generation of effector CD4+ T cells by promoting miR-124-mediated suppression of SOCS5. Science signaling 53 24619648
2019 MiR-9-5p could promote angiogenesis and radiosensitivity in cervical cancer by targeting SOCS5. European review for medical and pharmacological sciences 51 31539118
2019 LncRNA FER1L4 induces apoptosis and suppresses EMT and the activation of PI3K/AKT pathway in osteosarcoma cells via inhibiting miR-18a-5p to promote SOCS5. Gene 50 31473323
2018 A novel SOCS5/miR-18/miR-25 axis promotes tumorigenesis in liver cancer. International journal of cancer 46 30191950
2019 MiR-151a-3p Promotes Postmenopausal Osteoporosis by Targeting SOCS5 and Activating JAK2/STAT3 Signaling. Rejuvenation research 40 31411118
2013 Suppressor of Cytokine Signaling (SOCS) 5 utilises distinct domains for regulation of JAK1 and interaction with the adaptor protein Shc-1. PloS one 37 23990909
2018 Angpt2 Induces Mesangial Cell Apoptosis through the MicroRNA-33-5p-SOCS5 Loop in Diabetic Nephropathy. Molecular therapy. Nucleic acids 34 30414568
2016 Deregulation of SOCS5 suppresses dendritic cell function in chronic lymphocytic leukemia. Oncotarget 32 27317770
2020 lncRNA HAND2-AS1 Inhibits Liver Cancer Cell Proliferation and Migration by Upregulating SOCS5 to Inactivate the JAK-STAT Pathway. Cancer biotherapy & radiopharmaceuticals 31 32155348
2019 BRM transcriptionally regulates miR-302a-3p to target SOCS5/STAT3 signaling axis to potentiate pancreatic cancer metastasis. Cancer letters 30 30790683
2019 Epigenetic silencing of SOCS5 potentiates JAK-STAT signaling and progression of T-cell acute lymphoblastic leukemia. Cancer science 29 30974024
2011 SOCS5 and SOCS6 have similar expression patterns in normal and cancer tissues. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 28 22081311
2021 LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis. Bioengineered 25 34666613
2019 Long noncoding RNA TUSC7 inhibits cell proliferation, migration and invasion by regulating SOCS4 (SOCS5) expression through targeting miR-616 in endometrial carcinoma. Life sciences 25 31200002
2018 Upregulation of miR-132 contributes to the pathophysiology of COPD via targeting SOCS5. Experimental and molecular pathology 24 30292646
2021 Leonurine-Repressed miR-18a-5p/SOCS5/JAK2/STAT3 Axis Activity Disrupts CML malignancy. Frontiers in pharmacology 21 33935775
2022 Stellate ganglion block relieves acute lung injury induced by severe acute pancreatitis via the miR-155-5p/SOCS5/JAK2/STAT3 axis. European journal of medical research 19 36333771
2020 Long non-coding RNA HCG11 sponging miR-522-3p inhibits the tumorigenesis of non-small cell lung cancer by upregulating SOCS5. Thoracic cancer 19 32844573
2022 Mycoplasma gallisepticum escapes the host immune response via gga-miR-365-3p/SOCS5/STATs axis. Veterinary research 17 36471418
2020 Long noncoding RNA HAND2-AS1 reduced the viability of hepatocellular carcinoma via targeting microRNA-300/SOCS5 axis. Hepatobiliary & pancreatic diseases international : HBPD INT 17 32224127
2020 LncRNA CASC2 inhibits cell proliferation, metastasis and EMT through miR-18a/SOCS5 axis in cholangiocarcinoma. European review for medical and pharmacological sciences 17 32894543
2015 Structure and Functional Characterization of the Conserved JAK Interaction Region in the Intrinsically Disordered N-Terminus of SOCS5. Biochemistry 17 26173083
2019 miR-26a Inhibits Feline Herpesvirus 1 Replication by Targeting SOCS5 and Promoting Type I Interferon Signaling. Viruses 16 31861450
2022 Circular RNA circ_0047744 suppresses the metastasis of pancreatic ductal adenocarcinoma by regulating the miR-21/SOCS5 axis. Biochemical and biophysical research communications 13 35334414
2020 LINC00668 Modulates SOCS5 Expression Through Competitively Sponging miR-518c-3p to Facilitate Glioma Cell Proliferation. Neurochemical research 13 32279214
2019 Correction: SOCS5 inhibition induces autophagy to impair metastasis in hepatocellular carcinoma cells via the PI3K/Akt/mTOR pathway. Cell death & disease 13 31641102
2022 SOCS5 contributes to temozolomide resistance in glioblastoma by regulating Bcl-2-mediated autophagy. Bioengineered 12 35730472
2021 The LINC01119-SOCS5 axis as a critical theranostic in triple-negative breast cancer. NPJ breast cancer 12 34059683
2005 SOCS5 mRNA levels in peripheral blood mononuclear cells (PBMC): a potential bio-marker for monitoring response of uveitis patients to Daclizumab therapy. Journal of autoimmunity 12 15725575
2021 Salidroside Attenuates Airway Inflammation and Remodeling via the miR-323-3p/SOCS5 Axis in Asthmatic Mice. International archives of allergy and immunology 11 34856542
2007 PMA activates Stat3 in the Jak/Stat pathway and induces SOCS5 in rat brain astrocytes. Molecules and cells 11 17464217
2020 miR-101 inhibits feline herpesvirus 1 replication by targeting cellular suppressor of cytokine signaling 5 (SOCS5). Veterinary microbiology 10 32456815
2019 Molecular Cloning and Expression Analysis of Three Suppressors of Cytokine Signaling Genes (SOCS5, SOCS6, SOCS7) in the Mealworm Beetle Tenebrio molitor. Insects 10 30884777
2024 SOCS5-RBMX stimulates SREBP1-mediated lipogenesis to promote metastasis in steatotic HCC with HBV-related cirrhosis. NPJ precision oncology 9 38429411
2023 Sequential inspiratory muscle exercise-noninvasive positive pressure ventilation alleviates oxidative stress in COPD by mediating SOCS5/JAK2/STAT3 pathway. BMC pulmonary medicine 9 37828534
2019 Differential Transcription of SOCS5 and SOCS7 in Multiple Sclerosis Patients Treated with Interferon Beta or Glatiramer Acetate. International journal of molecular sciences 9 31905601
2011 SOCS3 and SOCS5 mRNA expressions may predict initial steroid response in nephrotic syndrome children. Folia histochemica et cytobiologica 9 22252769
2023 Resistin stimulates PC-3 prostate cancer cell growth through stimulation of SOCS3 and SOCS5 genes. Experimental biology and medicine (Maywood, N.J.) 8 37646261
2020 miR-802 participates in the inflammatory process of inflammatory bowel disease by suppressing SOCS5. Bioscience reports 8 32211804
2000 Cloning and expression of CIS6, chromosome assignment to 3p22 and 2p21 by in situ hybridization. Cytogenetics and cell genetics 8 10773671
2023 Adenovirus-IL-10 relieves chronic rejection after mouse heart transplantation by inhibiting miR-155 and activating SOCS5. International journal of medical sciences 7 36794154
2022 SOCS5 knockdown suppresses metastasis of hepatocellular carcinoma by ameliorating HIF-1α-dependent mitochondrial damage. Cell death & disease 7 36319626
2005 Milk fat synthesis is unaffected by abomasal infusion of the conjugated diene 18:3 isomers cis-6,trans-10, cis-12 and cis-6,trans-8,cis-12. Lipids 7 15825834
2024 SOCS5, targeted by miR-155-5p, plays a negative regulatory role in pulmonary hypertension through inhibiting JAK2/STAT3 signaling pathway. BMC pulmonary medicine 5 38267898
2022 SP1/miR-92a-1-5p/SOCS5: A novel regulatory axis in feline panleukopenia virus replication. Veterinary microbiology 5 36037621
2022 miR-155-1 as a positive factor for novel duck reovirus replication by regulating SOCS5-mediated interferons. Virus research 4 36384170
2023 Reduced NR2F2 Expression in the Host Response to Infectious Bursal Disease Virus Infection Suppressed Viral Replication by Enhancing Type I Interferon Expression by Targeting SOCS5. Journal of virology 3 37358466
2020 The overexpression of miRNA-212-5p inhibited the malignant proliferation of liver cancer cells HepG2 and the tumor formation in nude mice with transplanted tumor through down-regulating SOCS5. Translational cancer research 3 35117765
2023 Evaluation of SOCS5 mRNA and its association with serum IL-12 levels and rs41379147 SNP in various subsets of allergic disorders: A case control study. Molecular immunology 2 37672963
2021 Author Correction: LncRNA CASC2 inhibits cell proliferation, metastasis and EMT through miR-18a/SOCS5 axis in cholangiocarcinoma. European review for medical and pharmacological sciences 2 33660836
2019 Association of SOCS5 gene polymorphism with allergic bronchial asthma. Terapevticheskii arkhiv 2 31094455
2017 [Role of negative regulators of SOCS1, SOCS3, and SOCS5 gene transcription in the negative cell signaling regulation system in asthma]. Terapevticheskii arkhiv 2 28378729
2022 Circ_0031027 adjusts the advancement of cervical cancer by miR-587/SOCS5 axis. American journal of reproductive immunology (New York, N.Y. : 1989) 1 36315981
2026 Morinda officinalis polysaccharide improves osteoporosis by enhancing m⁶A-modified SOCS5 mRNA stability via regulating the hsa_circ_0001165/IGF2BP2 axis. Molecular genetics and genomics : MGG 0 41843192
2026 Mechanistic insights into SOCS5-related DNA damage and cellular senescence in diabetic retinopathy. Cell death discovery 0 41922309
2025 Psoralen promotes SOCS5 to inhibit JAK/STAT3 to alleviate cartilage degeneration in knee osteoarthritis. Phytomedicine : international journal of phytotherapy and phytopharmacology 0 41385946
2013 [Association of polymorphism Rs6737848 in the Socs5 gene with bronchial asthma]. Vestnik Rossiiskoi akademii meditsinskikh nauk 0 24340963

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