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{{Infobox_gene}}

细胞因子信号传导抑制因子3(SOCS3或 SOCS-3)是一种在人体内由 SOCS3[[基因]]编码的[[蛋白质|蛋白]]。<ref name="pmid9266833">{{Cite journal|title=Cloning and functional analysis of new members of STAT induced STAT inhibitor (SSI) family: SSI-2 and SSI-3|date=September 1997|journal=Biochem Biophys Res Commun|issue=1|doi=10.1006/bbrc.1997.7080|volume=237|pages=79–83|pmc=|pmid=9266833}}</ref><ref name="pmid9344848">{{Cite journal|title=Cloning and characterization of novel CIS family genes|date=November 1997|journal=Biochem Biophys Res Commun|issue=2|doi=10.1006/bbrc.1997.7484|volume=239|pages=439–46|pmc=|pmid=9344848}}</ref> 该基因编码 STAT- 诱导的 STAT 抑制子(SSI)，也可称为[[细胞因子]]信号转导(SOCS)家族抑制子，的一个成员。 SSI 家族成员是可由细胞因子诱导的细胞因子信号转导负调节因子。

== 功能 ==
SOCS3基因的表达可由多种细胞因子的诱导，包括 IL-6，[[IL-10]]，[[干扰素-γ]](IFN-γ)。

在 IL-6，Epo，GCSF 和瘦素的信号传导中，已发现SOCS3在各自的细胞因子受体上的结合对 SOCS3的抑制功能而言是至关重要的。

SOCS3的过表达会抑制[[脂肪組織|脂肪组织]]和[[肝脏]][[胰岛素]]信号转导，但对肌肉则不然。<ref name="pmid22961088">{{Cite journal|title=Deletion of skeletal muscle SOCS3 prevents insulin resistance in obesity|url=http://diabetes.diabetesjournals.org/content/62/1/56.long|journal=[[Diabetes (journal)|Diabetes]]|issue=1|doi=10.2337/db12-0443|year=2013|volume=62|pages=56–64|pmc=3526029|pmid=22961088|access-date=2018-11-22|archive-date=2018-11-23|archive-url=https://web.archive.org/web/20181123023000/http://diabetes.diabetesjournals.org/content/62/1/56.long|dead-url=no}}</ref> 但是在小鼠[[骨骼肌]]中敲除 SOCS3可以保护小鼠免于肥胖相关的[[胰岛素抵抗]]。<ref name="pmid22961088" />

由于[[神经酰胺]]合成的增加，SOCS3会增加[[瘦素]]抵抗和胰岛素抵抗。<ref name="pmid19435851">{{Cite journal|title=Central role of ceramide biosynthesis in body weight regulation, energy metabolism, and the metabolic syndrome|url=http://ajpendo.physiology.org/content/297/1/E211.long|journal=[[American Journal of Physiology]]|issue=1|doi=10.1152/ajpendo.91014.2008|year=2009|volume=297|pages=E211-E224|pmc=2711669|pmid=19435851|id=|access-date=2018-11-22|archive-date=2016-08-10|archive-url=https://web.archive.org/web/20160810012845/http://ajpendo.physiology.org/content/297/1/E211.long|dead-url=no}}</ref> 因此，研究已表明去除 SOCS 基因可以预防[[肥胖症]]患者的胰岛素抵抗<ref name="pmid22961088">{{Cite journal|title=Deletion of skeletal muscle SOCS3 prevents insulin resistance in obesity|url=http://diabetes.diabetesjournals.org/content/62/1/56.long|journal=[[Diabetes (journal)|Diabetes]]|issue=1|doi=10.2337/db12-0443|year=2013|volume=62|pages=56–64|pmc=3526029|pmid=22961088}}</ref>

对该小鼠中基因的同源基因的研究表明，该基因在胎儿肝脏[[造血]]和[[胎盘]]发育的负调控中发挥作用。<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=9021|title=Entrez Gene: SOCS3 suppressor of cytokine signaling 3|accessdate=|archive-date=2010-03-07|archive-url=https://web.archive.org/web/20100307221611/http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=9021|dead-url=no}}</ref>

SOCS3蛋白能与[[JAK激酶|JAK]]2结合，抑制其活性。

== 相互作用 ==
已经证明 SOCS3可以与下列物质相互作用:

* [[促红细胞生成素]]受体<ref name="pmid10882725">{{Cite journal|title=CIS3/SOCS-3 suppresses erythropoietin (EPO) signaling by binding the EPO receptor and JAK2|url=https://archive.org/details/sim_journal-of-biological-chemistry_2000-09-22_275_38/page/29338|date=September 2000|journal=J. Biol. Chem.|issue=38|doi=10.1074/jbc.M003456200|volume=275|pages=29338–47|pmid=10882725}}</ref><ref name="pmid12027890">{{Cite journal|title=A new high affinity binding site for suppressor of cytokine signaling-3 on the erythropoietin receptor|date=May 2002|journal=Eur. J. Biochem.|issue=10|doi=10.1046/j.1432-1033.2002.02916.x|volume=269|pages=2516–26|pmid=12027890}}</ref>
* [[糖蛋白]]130<ref name="pmid12403768" />
* [[胰岛素样生长因子1受体]]<ref name="pmid11071852">{{Cite journal|title=Suppressor of cytokine signaling (SOCS)-3 protein interacts with the insulin-like growth factor-I receptor|date=November 2000|journal=Biochem. Biophys. Res. Commun.|issue=1|doi=10.1006/bbrc.2000.3762|volume=278|pages=38–43|pmid=11071852}}</ref>
* [[JAK激酶|JAK]]2<ref name="pmid9344848">{{Cite journal|title=Cloning and characterization of novel CIS family genes|date=November 1997|journal=Biochem Biophys Res Commun|issue=2|doi=10.1006/bbrc.1997.7484|volume=239|pages=439–46|pmc=|pmid=9344848}}</ref><ref name="pmid10882725" /><ref name="pmid10421843">{{Cite journal|title=Cytokine-inducible SH2 protein-3 (CIS3/SOCS3) inhibits Janus tyrosine kinase by binding through the N-terminal kinase inhibitory region as well as SH2 domain|date=June 1999|journal=Genes Cells|issue=6|doi=10.1046/j.1365-2443.1999.00263.x|volume=4|pages=339–51|pmid=10421843}}</ref>
* [[蛋白酪氨酸磷酸酶|PTP]]N11<ref name="pmid12403768">{{Cite journal|title=SHP2 and SOCS3 contribute to Tyr-759-dependent attenuation of interleukin-6 signaling through gp130|url=https://archive.org/details/sim_journal-of-biological-chemistry_2003-01-03_278_1/page/660|date=January 2003|journal=J. Biol. Chem.|issue=1|doi=10.1074/jbc.M210552200|volume=278|pages=661–71|pmid=12403768}}</ref>
* RAS p21蛋白激活因子1<ref name="pmid11331873">{{Cite journal|title=Tyrosine-phosphorylated SOCS-3 inhibits STAT activation but binds to p120 RasGAP and activates Ras|date=May 2001|journal=Nat. Cell Biol.|issue=5|doi=10.1038/35074525|volume=3|pages=460–5|pmid=11331873}}</ref>

== 调控 ==
有部分证据表明 SOCS3的表达受[[小分子核糖核酸]] miR-203的调控。<ref name="pmid18483491">{{Cite journal|title=miR-203 represses 'stemness' by repressing DeltaNp63.|journal=Cell Death Differ|issue=7|doi=10.1038/cdd.2008.69|year=2008|volume=15|pages=1187–95|pmid=18483491}}</ref><ref name="pmid20698882">{{Cite journal|title=The expression of microRNA-203 during human skin morphogenesis.|journal=Exp Dermatol|issue=9|doi=10.1111/j.1600-0625.2010.01118.x|year=2010|volume=19|pages=854–6|pmid=20698882}}</ref>

== 参见 ==

* [[SOCS]]
* [[JAK-STAT信号通路]]

== 参考文献 ==
<references group="" responsive=""></references>

== 扩展阅读 ==

* Yasukawa H, Sasaki A, Yoshimura A (2000). "Negative regulation of cytokine signaling pathways". Annu. Rev. Immunol. 18: 143–64. [[DOI|doi:10.1146/annurev.immunol.18.1.143]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/10837055 10837055]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/10837055 |date=20181123065522 }}.
* Kile BT, Schulman BA, Alexander WS, Nicola NA, Martin HM, Hilton DJ (2002). "The SOCS box: a tale of destruction and degradation". Trends Biochem. Sci. 27 (5): 235–41. [[DOI|doi:]][[doi:10.1016/S0968-0004(02)02085-6|10.1016/S0968-0004(02)02085-6]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/12076535 1276535]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/12076535 |date=20181123022802 }}.
* Zhang JG, Farley A, Nicholson SE, Willson TA, Zugaro LM, Simpson RJ, Moritz RL, Cary D, Richardson R, Hausmann G, Kile BJ, Kent SB, Alexander WS, Metcalf D, Hilton DJ, Nicola NA, Baca M (1999). [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC26738 "The conserved SOCS box motif in suppressors of cytokine signaling binds to elongins B and C and may couple bound proteins to proteasomal degradation"]. Proc. Natl. Acad. Sci. U.S.A. 96 (5): 2071–6. [[DOI|doi]]:[[doi:10.1073/pnas.96.5.2071|10.1073/pnas.96.5.2071]]. PMC [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC26738 26738]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/10051596 10051596]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/10051596 |date=20181123022925 }}.
* Sasaki A, Yasukawa H, Suzuki A, Kamizono S, Syoda T, Kinjyo I, Sasaki M, Johnston JA, Yoshimura A (1999). "Cytokine-inducible SH2 protein-3 (CIS3/SOCS3) inhibits Janus tyrosine kinase by binding through the N-terminal kinase inhibitory region as well as SH2 domain". Genes Cells. 4 (6): 339–51. [[doi]]:[[doi:10.1046/j.1365-2443.1999.00263.x|10.1046/j.1365-2443.1999.00263.x]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/10421843 10421843]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/10421843 |date=20181123065541 }}.
* Marine JC, McKay C, Wang D, Topham DJ, Parganas E, Nakajima H, Pendeville H, Yasukawa H, Sasaki A, Yoshimura A, Ihle JN (1999). "SOCS3 is essential in the regulation of fetal liver erythropoiesis". Cell. 98 (5): 617–27. [[doi]]:[[10.1016/S0092-8674(00)80049-5]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/10490101 10490101]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/10490101 |date=20181123022820 }}.
* Schmitz J, Weissenbach M, Haan S, Heinrich PC, Schaper F (2000). "SOCS3 exerts its inhibitory function on interleukin-6 signal transduction through the SHP2 recruitment site of gp130". J. Biol. Chem. 275 (17): 12848–56. [[doi]]:[[doi:10.1074/jbc.275.17.12848|10.1074/jbc.275.17.12848]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/10777583 10777583]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/10777583 |date=20181123065610 }}.
* Ram PA, Waxman DJ (2000). "SOCS/CIS protein inhibition of growth hormone-stimulated STAT5 signaling by multiple mechanisms". J. Biol. Chem. 274 (50): 35553–61. [[doi]]:[[doi:10.1074/jbc.274.50.35553|10.1074/jbc.274.50.35553]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/10585430 10585430]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/10585430 |date=20181123023005 }}.
* Sasaki A, Yasukawa H, Shouda T, Kitamura T, Dikic I, Yoshimura A (2000). "CIS3/SOCS-3 suppresses erythropoietin (EPO) signaling by binding the EPO receptor and JAK2". J. Biol. Chem. 275 (38): 29338–47. [[doi]]:[[doi:10.1074/jbc.M003456200|10.1074/jbc]].[[doi:10.1074/jbc.M003456200|M003456200]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/10882725 10882725]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/10882725 |date=20181123065552 }}.
* Anhuf D, Weissenbach M, Schmitz J, Sobota R, Hermanns HM, Radtke S, Linnemann S, Behrmann I, Heinrich PC, Schaper F (2000). "Signal transduction of IL-6, leukemia-inhibitory factor, and oncostatin M: structural receptor requirements for signal attenuation". J. Immunol. 165 (5): 2535–43. [[doi]]:[[doi:10.4049/jimmunol.165.5.2535|10.4049/jimmunol.165.5.2535]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/10946280 10946280]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/10946280 |date=20181123022958 }}.
* Bjorbak C, Lavery HJ, Bates SH, Olson RK, Davis SM, Flier JS, Myers MG (2001). "SOCS3 mediates feedback inhibition of the leptin receptor via Tyr985". J. Biol. Chem. 275 (51): 40649–57. [[doi]]:[[doi:10.1074/jbc.M007577200|10.1074/jbc]].[[doi:10.1074/jbc.M007577200|M007577200]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/11018044 11018044]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/11018044 |date=20181123022739 }}.
* Shen X, Hong F, Nguyen VA, Gao B (2000). "IL-10 attenuates IFN-alpha-activated STAT1 in the liver: involvement of SOCS2 and SOCS3". FEBS Lett. 480 (2–3): 132–6. [[doi]]:[[doi:10.1016/S0014-5793(00)01905-0|10.1016/S0014-5793(00)01905-0]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/11034314 11034314]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/11034314 |date=20181123022927 }}.
* Dey BR, Furlanetto RW, Nissley P (2001). "Suppressor of cytokine signaling (SOCS)-3 protein interacts with the insulin-like growth factor-I receptor". Biochem. Biophys. Res. Commun. 278 (1): 38–43. [[doi]]:[[doi:10.1006/bbrc.2000.3762|10.1006/bbrc.2000.3762]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/11071852 11071852]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/11071852 |date=20181123023110 }}.
* Hartley JL, Temple GF, Brasch MA (2001). [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC310948 "DNA cloning using in vitro site-specific recombination"] {{Wayback|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC310948 |date=20220424204317 }}. Genome Res. 10 (11): 1788–95. [[doi]]:[[doi:10.1101/gr.143000|10.1101/gr.143000]]. PMC [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC310948 310948] {{Wayback|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC310948 |date=20220424204317 }}. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/11076863 11076863]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/11076863 |date=20181123022814 }}.
* Cookson WO, Ubhi B, Lawrence R, Abecasis GR, Walley AJ, Cox HE, Coleman R, Leaves NI, Trembath RC, Moffatt MF, Harper JI (2001). "Genetic linkage of childhood atopic dermatitis to psoriasis susceptibility loci". Nat. Genet. 27 (4): 372–3. [[doi]]:[[doi:10.1038/86867|10.1038/86867]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/11279517 11279517]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/11279517 |date=20181123065513 }}.
* Cacalano NA, Sanden D, Johnston JA (2001). "Tyrosine-phosphorylated SOCS-3 inhibits STAT activation but binds to p120 RasGAP and activates Ras". Nat. Cell Biol. 3 (5): 460–5. [[doi]]:[[doi:10.1038/35074525|10.1038/35074525]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/11331873 11331873]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/11331873 |date=20181123022755 }}.
* Roberts AW, Robb L, Rakar S, Hartley L, Cluse L, Nicola NA, Metcalf D, Hilton DJ, Alexander WS (2001). [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC55419 "Placental defects and embryonic lethality in mice lacking suppressor of cytokine signaling 3"]. Proc. Natl. Acad. Sci. U.S.A. 98 (16): 9324–9. [[doi]]:[[doi:10.1073/pnas.161271798|10.1073/pnas.161271798]]. PMC [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC55419 55419]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/11481489 11481489]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/11481489 |date=20181123023026 }}.
* Dif F, Saunier E, Demeneix B, Kelly PA, Edery M (2001). "Cytokine-inducible SH2-containing protein suppresses PRL signaling by binding the PRL receptor". Endocrinology. 142 (12): 5286–93. [[doi]]:[[doi:10.1210/endo.142.12.8549|10.1210/endo.142.12.8549]]. [[PMID]][[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/11713228 11713228]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/11713228 |date=20181123023130 }}.
* Bode JG, Ludwig S, Freitas CA, Schaper F, Ruhl M, Melmed S, Heinrich PC, Häussinger D (2002). "The MKK6/p38 mitogen-activated protein kinase pathway is capable of inducing SOCS3 gene expression and inhibits IL-6-induced transcription". Biol. Chem. 382 (10): 1447–53. [[doi]]:[[doi:10.1515/BC.2001.178|10.1515/BC.2001.178]]. [[PMID]] [https://www.ncbi.nlm.nih.gov/pubmed/11727828 11727828]{{Wayback|url=https://www.ncbi.nlm.nih.gov/pubmed/11727828 |date=20181123022849 }}.

{{JAK-STAT信号通路}}
[[Category:位於17號人類染色體的基因]]
[[Category:有未审阅翻译的页面]]

SOCS3 - 版本历史

imported>InternetArchiveBot：​Add 2 books for verifiability (20251017sim)) #IABot (v2.0.9.5) (GreenC bot

imported>InternetArchiveBot：Add 2 books for verifiability (20251017sim)) #IABot (v2.0.9.5) (GreenC bot