Affinage

SOCS5

Suppressor of cytokine signaling 5 · UniProt O75159

Length
536 aa
Mass
61.2 kDa
Annotated
2026-04-28
65 papers in source corpus 16 papers cited in narrative 16 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SOCS5 is a multifunctional negative regulator of cytokine and growth factor signaling that modulates JAK-STAT, EGFR, and PI3K/Akt/mTOR pathways across immune and epithelial cell contexts. Its N-terminal JAK Interaction Region (JIR), which contains preformed structural elements within an otherwise disordered domain, directly binds and inhibits JAK1 and JAK2 kinase activity, while its SH2 domain engages phosphotyrosine motifs on adaptors such as Shc-1 (pY317), and its SOCS box recruits E3 ubiquitin ligase machinery to promote proteasomal degradation of the EGFR (PMID:23990909, PMID:15695332, PMID:26173083). SOCS5 inhibits IL-4Rα-STAT6 signaling to suppress Th2 differentiation (PMID:12242343), restricts influenza A virus replication via EGFR pathway regulation in airway epithelium (PMID:28195529), and its SH2 domain interacts with the RNA-binding protein RBMX to co-activate SREBP1-driven de novo lipogenesis in hepatocellular carcinoma (PMID:38429411). Epigenetic silencing of SOCS5 in T-ALL activates JAK-STAT signaling and accelerates leukemia progression, while in HCC, SOCS5 modulates PI3K/Akt/mTOR-dependent autophagy and HIF-1α-mediated hypoxic responses (PMID:30974024, PMID:31406106, PMID:36319626).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2000 Medium

    Identification of SOCS5 as a new CIS/SOCS family member with a conserved SH2 domain and SOCS box established it as a candidate cytokine signaling regulator.

    Evidence cDNA cloning, Northern blot, and chromosomal mapping in human tissues and cell lines

    PMID:10773671

    Open questions at the time
    • No signaling function demonstrated
    • No binding partners identified
    • No loss-of-function data
  2. 2002 High

    The first functional role was established: SOCS5 binds IL-4Rα and suppresses IL-4/STAT6 signaling, positioning it as a regulator of Th1/Th2 balance.

    Evidence Co-immunoprecipitation and transgenic mouse overexpression model with Th2 differentiation assays

    PMID:12242343

    Open questions at the time
    • Mechanism of IL-4Rα binding unclear (phosphorylation-independent)
    • Endogenous requirement not tested via loss-of-function
  3. 2004 High

    Genetic knockout unexpectedly revealed that SOCS5 is dispensable for lymphocyte development and Th1/Th2 differentiation under standard conditions, suggesting functional redundancy in immune cells.

    Evidence Socs5-/- mice with comprehensive immune phenotyping, Th differentiation assays, and Leishmania major infection

    PMID:15199163

    Open questions at the time
    • Redundant SOCS family members not identified
    • Non-immune phenotypes not examined
    • Stress or disease-specific requirements not tested
  4. 2005 High

    SOCS5 was shown to associate with and inhibit EGFR signaling in a SOCS box-dependent manner, establishing a second major signaling axis and linking SOCS5 to receptor tyrosine kinase regulation via ubiquitin-proteasome degradation.

    Evidence Co-immunoprecipitation and SOCS box deletion mutagenesis with mitogenic response assays in engineered cell lines

    PMID:15695332

    Open questions at the time
    • Direct ubiquitination of EGFR not demonstrated
    • E3 ligase complex identity not resolved
    • EGF-independent binding mechanism unclear
  5. 2013 High

    The N-terminal JIR was identified as a novel domain that directly binds and inhibits JAK1/JAK2 kinase activity via a mechanism distinct from SOCS1/3, and the SH2 domain was shown to bind Shc-1 pY317, unifying JAK and growth factor suppressive activities.

    Evidence In vitro kinase assays, domain mutagenesis, peptide binding studies

    PMID:23990909

    Open questions at the time
    • Selectivity mechanism for JAK1/2 over JAK3/TYK2 not resolved
    • In vivo contribution of JIR versus SH2 domain not dissected
  6. 2014 High

    SOCS5 was placed downstream of MeCP2/miR-124 regulation, revealing that SOCS5 accumulation inhibits STAT1 and STAT3 activation and impairs Th1/Th17 differentiation — broadening its role beyond Th2 suppression.

    Evidence MeCP2 knockdown, miR-124 functional assays, STAT phosphorylation Western blots, in vivo T cell differentiation

    PMID:24619648

    Open questions at the time
    • Whether SOCS5 directly inhibits STAT1/3 or acts via JAK not resolved
    • Relative contribution of miR-124 versus other miRNAs unclear
  7. 2015 High

    NMR structural analysis of the JIR revealed preformed α-helical and extended structural elements within the otherwise disordered N-terminus, and identified Ser211 phosphorylation as a modulator of JAK binding, providing the first structural basis for SOCS5-JAK interaction.

    Evidence NMR spectroscopy (chemical shifts, relaxation, NOE) with site-directed mutagenesis

    PMID:26173083

    Open questions at the time
    • Full structure of JIR-JAK complex not solved
    • Kinase responsible for Ser211 phosphorylation unknown
    • Functional consequence of Ser211 phosphorylation in cells not shown
  8. 2016 Medium

    In CLL, STAT3-driven SOCS5 induction in monocytes was shown to decouple IL-4R/STAT6 signaling and impair dendritic cell differentiation, demonstrating a disease-relevant immunosuppressive circuit.

    Evidence Patient-derived monocytes, IL-10 treatment, Western blot, flow cytometry, cytokine secretion assays

    PMID:27317770

    Open questions at the time
    • Single lab finding in CLL
    • Causal role of SOCS5 not confirmed by genetic manipulation in patient cells
  9. 2017 High

    SOCS5 was shown to restrict influenza A virus replication through EGFR signaling regulation in airway epithelium, establishing an in vivo non-immune function for SOCS5 with pathophysiological relevance.

    Evidence Socs5-/- mice with viral titre measurement, weight loss phenotyping, primary epithelial cell assays

    PMID:28195529

    Open questions at the time
    • Precise EGFR-dependent mechanism in epithelial antiviral defense not fully delineated
    • Whether SOCS5 acts cell-autonomously versus via paracrine signals not resolved
  10. 2018 Medium

    SOCS5 was positioned in an miR-18a/miR-25–SOCS5–TSC1–mTOR tumor-suppressive axis in HCC, linking SOCS5 loss to mTOR activation via reduced TSC1 levels.

    Evidence miRNA target validation by luciferase assay, SOCS5 overexpression/knockdown, mTOR/TSC1 pathway analysis

    PMID:30191950

    Open questions at the time
    • Mechanism by which SOCS5 maintains TSC1 levels not defined
    • Single lab, not independently confirmed
  11. 2019 Medium

    SOCS5 was shown to regulate PI3K/Akt/mTOR-dependent autophagy and promote HCC metastasis, and separately, epigenetic silencing of SOCS5 in T-ALL was found to activate JAK-STAT signaling and accelerate leukemia, establishing SOCS5 as a context-dependent oncogene and tumor suppressor.

    Evidence SOCS5 knockdown/overexpression with autophagy/migration assays and in vivo models (HCC); DNA methylation/chromatin studies with xenograft models (T-ALL)

    PMID:30974024 PMID:31406106

    Open questions at the time
    • Context-dependent oncogenic versus tumor-suppressive roles not mechanistically reconciled
    • Direct SOCS5 substrate in mTOR pathway unidentified
  12. 2022 Medium

    SOCS5 was found to promote Bcl-2 transcription driving autophagy-mediated temozolomide resistance in glioblastoma, and separately to sustain HIF-1α via PI3K/Akt/mTOR to drive hypoxic invasion in HCC, revealing SOCS5 as a regulator of stress-adaptive transcriptional programs.

    Evidence Knockdown/overexpression with Bcl-2 transcription and autophagy assays (GBM); CoCl2 hypoxia model, pharmacological rescue, in vivo metastasis models (HCC)

    PMID:35730472 PMID:36319626

    Open questions at the time
    • Mechanism by which SOCS5 activates Bcl-2 transcription unknown
    • Whether SOCS5 acts directly on PI3K/Akt or via intermediate signaling not resolved
    • Findings from single labs
  13. 2024 High

    The SH2 domain of SOCS5 was shown to directly bind RBMX via specific residues (Y413, D443), and this complex co-activates SREBP1-driven de novo lipogenesis in HCC, revealing a novel non-canonical function of SOCS5 in metabolic gene regulation.

    Evidence Co-IP, GST pulldown, site-directed mutagenesis, proteomics, metabolomics, promoter assays, in vivo experiments

    PMID:38429411

    Open questions at the time
    • Whether RBMX interaction is relevant outside HCC unknown
    • How the SOCS5-RBMX complex activates SREBP1 transcription mechanistically not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how SOCS5 toggles between tumor-suppressive (T-ALL, immune contexts) and oncogenic (HCC, GBM) functions, whether the JIR and SH2 domain mediate separable signaling outputs in vivo, and what structural basis governs the full SOCS5-JAK or SOCS5-RBMX complexes.
  • No full-length SOCS5 structure available
  • JIR-JAK complex structure not solved
  • Context-dependent tumor-suppressive versus oncogenic switching mechanism unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4 GO:0140110 transcription regulator activity 2
Localization
GO:0005829 cytosol 3
Pathway
R-HSA-162582 Signal Transduction 7 R-HSA-168256 Immune System 4 R-HSA-1643685 Disease 3 R-HSA-9612973 Autophagy 2 R-HSA-1430728 Metabolism 1 R-HSA-392499 Metabolism of proteins 1
Partners
EGFRIL4RJAK1JAK2RBMXSHC1

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 SOCS5 protein is preferentially expressed in Th1 cells and interacts directly with the cytoplasmic region of the IL-4Rα chain in a phosphorylation-independent manner, resulting in inhibition of IL-4-mediated STAT6 activation and suppression of Th2 differentiation; transgenic mice constitutively expressing SOCS5 showed significantly reduced IL-4-mediated Th2 development. Co-immunoprecipitation, transgenic mouse model, flow cytometry, cytokine signaling 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 mitogenic signaling; this inhibition requires the SOCS5 SOCS box, suggesting it acts through SOCS box-recruited E3 ubiquitin ligase activity to promote proteasomal degradation of the EGF-R. Co-immunoprecipitation, engineered cell line constitutively expressing EGF-R and SOCS5 or SOCS5 deletion mutants, mitogenic response assays Proceedings of the National Academy of Sciences of the United States of America High 15695332
2013 SOCS5 contains a conserved JAK Interaction Region (JIR) in its N-terminus that directly binds JAK kinase domains; co-expression of SOCS5 specifically reduces JAK1 and JAK2 (but not JAK3 or TYK2) autophosphorylation and directly inhibits JAK1 kinase activity via a mechanism distinct from SOCS1/SOCS3. Additionally, the SOCS5 SH2 domain binds phosphoTyr317 of Shc-1 with high affinity, suggesting SOCS5 negatively regulates EGF/growth factor-driven Shc-1 signaling. In vitro kinase assays, co-immunoprecipitation, domain mutagenesis, peptide binding/SH2 domain interaction studies PloS one High 23990909
2015 The JAK Interaction Region (JIR) within the intrinsically disordered N-terminus of SOCS5 adopts preformed structural elements including an α-helix (residues 224-233), a turn, and an extended structure as determined by NMR; a phosphorylation site (Ser211) within the JIR modulates JAK binding. NMR spectroscopy (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, and restoration of SOCS5 levels restricts influenza virus infection. Socs5 knockout mouse model, viral titre measurement, weight loss phenotyping, primary epithelial cell assays eLife High 28195529
2014 MeCP2 promotes expression of miR-124, which suppresses translation of SOCS5 mRNA; loss of MeCP2 leads to SOCS5 accumulation, which in turn inhibits STAT1 and STAT3 activation and impairs Th1 and Th17 differentiation. MeCP2 knockdown, miR-124 functional assays, Western blot for SOCS5/STAT phosphorylation, Th1/Th17 differentiation assays in vitro and in vivo Science signaling High 24619648
2016 In chronic lymphocytic leukemia, STAT3-dependent upregulation of SOCS5 in monocytes decouples IL-4R signaling from STAT6 activation, impairing dendritic cell differentiation and reducing expression of HLA-DR, costimulatory molecules, and pro-inflammatory cytokines; IL-10 treatment of healthy donor monocytes mimics this effect via STAT3-dependent SOCS5 induction. Western blot, flow cytometry, cytokine secretion assays, IL-10 treatment experiments, patient-derived monocytes Oncotarget Medium 27317770
2019 SOCS5 overexpression promotes HCC cell migration and invasion by inactivating PI3K/Akt/mTOR-mediated autophagy; SOCS5 knockdown suppresses HCC metastasis in vitro and in vivo by activating this autophagy pathway. SOCS5 knockdown/overexpression, PI3K/Akt/mTOR pathway Western blot, autophagy assays, migration/invasion assays, in vivo metastasis model Cell death & disease Medium 31406106
2019 SOCS5 expression is epigenetically silenced in T-ALL by DNMT3A-mediated DNA methylation and MeCP2-mediated histone deacetylation; SOCS5 silencing activates JAK-STAT signaling and negatively regulates IL-7 and IL-4 receptors, accelerating leukemia engraftment and progression in a xenograft model. DNA methylation analysis, chromatin studies, SOCS5 knockdown/reconstitution, JAK-STAT signaling assays, human T-ALL xenograft mouse model Cancer science Medium 30974024
2024 The SOCS5 SH2 domain, specifically amino acids Y413 and D443, directly binds the RRM domain of RBMX; the SOCS5-RBMX complex co-stimulates the SREBP1 promoter to induce de novo lipogenesis and promote HCC metastasis. Mutations at Y413 and D443 abolish this interaction and reverse lipogenesis. Co-immunoprecipitation, GST pulldown, proteomics, metabolomics, promoter assays, site-directed mutagenesis, in vivo and in vitro experiments NPJ precision oncology High 38429411
2000 SOCS5 (CIS6) was cloned as a member of the CIS/SOCS family with a conserved central SH2 domain and SOCS box, and was assigned to human chromosomal bands 2p21 and 3p22; it is expressed in heart, muscle, spleen, thymus, and myeloma cell lines. cDNA cloning, Northern blot analysis, in situ hybridization Cytogenetics and cell genetics Medium 10773671
2004 SOCS5-deficient (Socs5-/-) mice are viable, healthy, and fertile with no abnormalities in lymphocyte compartments; SOCS5 is expressed in primary B and T cells but is dispensable for lymphocyte production, antigen/cytokine-induced proliferation, and Th1/Th2 differentiation under the conditions tested. Targeted gene disruption (knockout mouse), Mendelian ratio analysis, lymphocyte phenotyping, Th1/Th2 differentiation assays, Leishmania major infection model Molecular and cellular biology High 15199163
2018 miR-18a and miR-25 target SOCS5 in HCC; SOCS5 loss activates mTOR signaling by reducing TSC1 levels, promoting tumor growth, establishing a SOCS5/miR-18a/miR-25/TSC1/mTOR tumor-suppressive axis in liver cancer. miRNA target validation (luciferase reporter assay), SOCS5 overexpression/knockdown, mTOR/TSC1 pathway Western blot, HCC cell proliferation assays International journal of cancer Medium 30191950
2022 SOCS5 enhances transcription of Bcl-2, promoting Bcl-2-recruited autophagy and mediating temozolomide resistance in glioblastoma cells; SOCS5 knockdown inhibits TMZ chemoresistance by reducing Bcl-2-mediated autophagy. SOCS5 knockdown/overexpression, Bcl-2 transcription assays, autophagy assays, drug resistance functional assays Bioengineered Medium 35730472
2022 SOCS5 knockdown inhibits HIF-1α protein expression and resists hypoxia-induced mitochondrial damage in HCC cells; the mechanism involves inhibition of the PI3K/Akt/mTOR/HIF-1α signaling axis, suppressing hypoxia-driven invasion and migration. SOCS5 knockdown, CoCl2 hypoxia model, immunofluorescence, electron microscopy, rescue experiments with LY294002 and rapamycin, in vivo subcutaneous and lung metastasis models Cell death & disease Medium 36319626
2023 POU2F1 acts as an upstream transcriptional activator of SOCS5, and the POU2F1-SOCS5-CDKN1A axis drives diabetic retinopathy by promoting DNA damage and cellular senescence; SOCS5 knockdown reduces vascular leakage, apoptosis, and senescence in DR models. In vitro (HG-induced HRMECs) and in vivo (STZ-induced DR mice) models, SOCS5 knockdown, CDKN1A expression analysis, POU2F1 transcription factor studies Cell death discovery Medium 41922309

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 110 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 52 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 45 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 33 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
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 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 18 36333771
2022 Mycoplasma gallisepticum escapes the host immune response via gga-miR-365-3p/SOCS5/STATs axis. Veterinary research 17 36471418
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
2020 Long noncoding RNA HAND2-AS1 reduced the viability of hepatocellular carcinoma via targeting microRNA-300/SOCS5 axis. Hepatobiliary & pancreatic diseases international : HBPD INT 16 32224127
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
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
2020 LINC00668 Modulates SOCS5 Expression Through Competitively Sponging miR-518c-3p to Facilitate Glioma Cell Proliferation. Neurochemical research 12 32279214
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
2007 PMA activates Stat3 in the Jak/Stat pathway and induces SOCS5 in rat brain astrocytes. Molecules and cells 11 17464217
2021 Salidroside Attenuates Airway Inflammation and Remodeling via the miR-323-3p/SOCS5 Axis in Asthmatic Mice. International archives of allergy and immunology 10 34856542
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
2011 SOCS3 and SOCS5 mRNA expressions may predict initial steroid response in nephrotic syndrome children. Folia histochemica et cytobiologica 9 22252769
2024 SOCS5-RBMX stimulates SREBP1-mediated lipogenesis to promote metastasis in steatotic HCC with HBV-related cirrhosis. NPJ precision oncology 8 38429411
2023 Sequential inspiratory muscle exercise-noninvasive positive pressure ventilation alleviates oxidative stress in COPD by mediating SOCS5/JAK2/STAT3 pathway. BMC pulmonary medicine 8 37828534
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
2023 Resistin stimulates PC-3 prostate cancer cell growth through stimulation of SOCS3 and SOCS5 genes. Experimental biology and medicine (Maywood, N.J.) 7 37646261
2022 SOCS5 knockdown suppresses metastasis of hepatocellular carcinoma by ameliorating HIF-1α-dependent mitochondrial damage. Cell death & disease 7 36319626
2019 Differential Transcription of SOCS5 and SOCS7 in Multiple Sclerosis Patients Treated with Interferon Beta or Glatiramer Acetate. International journal of molecular sciences 7 31905601
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