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Validated All-in-One™ qPCR Primer for SOCS1(NM_003745.1) Search again
Product ID:
HQP021399
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AISIMD, CIS1, CISH1, JAB, SOCS-1, SSI-1, SSI1, TIP-3, TIP3
Gene Description:
suppressor of cytokine signaling 1
Target Gene Accession:
NM_003745.1(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes a member of the STAT-induced STAT inhibitor (SSI), also known as suppressor of cytokine signaling (SOCS), family. SSI family members are cytokine-inducible negative regulators of cytokine signaling. The expression of this gene can be induced by a subset of cytokines, including IL2, IL3 erythropoietin (EPO), CSF2/GM-CSF, and interferon (IFN)-gamma. The protein encoded by this gene functions downstream of cytokine receptors, and takes part in a negative feedback loop to attenuate cytokine signaling. Knockout studies in mice suggested the role of this gene as a modulator of IFN-gamma action, which is required for normal postnatal growth and survival. [provided by RefSeq].
Gene References into function
- In keratinocytes overexpressing SOCS-1, the IFN-gamma-induced transactivation of an IFN-gamma-responsive reporter gene is markedly inhibited, as are phosphorylation of IFN-gamma R alpha and activation of STAT1 and STAT3.
- Loss of function of SAOS-1 in collaboration with hematopoietic oncogenes facilitates tumor progression
- interacts with TRIM8/GERP RING finger protein
- SOCS1 is frequently silenced by methylation in multiple myeloma, which may impair negative regulation of the Jak/STAT pathway and result in greater responsiveness to cytokines
- inhibits interferon-gamma-induced activation of human keratinocytes
- Inactivation of this protein is associated with hypermethylation in human hepatoblastomas.
- Methylation of the SOCS1 gene, resulting in transcriptional silencing, has been found in 65% of hepatocellular carcinoma cases, correlates with cytogenetic abnormalities, and may play an important role in the development of the cancer.
- SOCS-1 gene associated with transcriptional silencing in pancreatic ductal neoplasms and may have growth-promoting effects; its methylation may be useful marker
- Is the SOCS-1 gene silenced by CpG methylation?
- SOCS1 has a role in mediating Janus kinase 2 ubiquitination/degradation downstream of the prolactin receptor and is regulated by SHP-2
- Methylation-mediated silencing of SOCS-1 gene is associated with hepatocellular carcinoma
- SOCS-1 is faintly expressed in the hippocampus under basal conditions following status epilepticus, corroborating the hypothesis that seizure-induced gp130 cytokines play a direct neuromodulatory role in the hippocampus.
- Up-regulation of suppressor of cytokine signaling 1 is associated with adult T-cell leukemia
- Three functional STAT6- interferon-gamma-activated sequence-binding motifs situated close to each other 600 bp upstream of the SOCS-1 transcriptional initiation site mediate IL-4-IL-13-induced SOCS-1 transcription.
- Methylation of SOCS1 was absent in both AML and ALL patients. Frequent methylation of SHP1, but not SOCS1, may be important in the pathogenesis, but not prognosis, of acute leukaemias.
- hypermethylated in multiple myeloma.
- SOCS1 overexpression increased Rb protein levels and suppressed proliferation of cervical cancer cell lines infected with HPV
- These findings suggested that SOCS-1 may act as a tumor suppressor in at least some colorectal cancers and that SOCS-1 methylation may be a particular phenomenon related to a nearly onset of colorectal cancer.
- this gene is silenced in a substantial portion of pancreatic cancers through mechanisms that cause methylation in the promoter region
- HSOCP-1 is involved in cell cycle control and apoptosis
- Severity of liver fibrosis is strongly correlated with SOCS1 gene methylation.
- Although the methylation frequency of SOCS-1 is low, the data of Fujitake et al. indicate role of JAK/STAT/SOCS pathway in gastrointestinal tumorigenesis.
- Aberrant methylation of SOCS-1 may be associated with hepatocarcinogenesis.
- Our results demonstrate that SOCS-1 and SOCS-3 proteins inhibit IFN-alpha-induced activation of the Jak-STAT pathway and expression of the antiviral proteins 2',5'-OAS and MxA.
- SOCS1 and SOCS2 but not SOCS3 suppressed the growth of ovarian and breast cancer cells.
- SOCS-1 is a progression marker of human melanoma and may downregulate biological responses by endogenous and/or therapeutically administered cytokines.
- Methylation of the SOCS-1 gene was associated with lymph node metastasis, advanced tumor stage and reduced expression of SOCS-1 in GC tissues.
- Data link SOCS-1 directly with the proteasome pathway and suggest another function for the SH2 domain of SOCS-1 in the regulation of Jak/STAT signaling.
- Egr-1 has roles in regulating both the basal and LPS-induced activity of the SOCS-1 promoter
- The insertion of amino acid exchanges into the kinase inhibitory regions of SOCS-1 demonstrated a requirement of these domains for a proper inhibitory function.
- Similar to SOCS-1, Tkip peptide binds to the autophosphorylation site of JAK2.
- IL-28A and IL-29 induced mRNA expression of the antiviral proteins 2',5'-OAS and MxA was abolished by overexpression of SOCS-1
- Suppressor of cytokine signaling-1 expression by infectivity-enhanced adenoviral vector inhibits IL-6-dependent proliferation of multiple myeloma cells.
- loss of SOCS-1 function either by mutation or by the complete deletion of the gene plays an important role in the dysregulation of JAK/STAT signaling in Karpas1106P and primary mediastinal b-cell lymphoma
- Data suggest that SOCS1 functions as a negative regulator in TNF-induced inflammation and activation of c-jun N-terminal kinase in endothelial cells, in part by inducing ASK1 degradation.
- Results suggest a novel interaction between the SOCS1 and SOCS3 proteins and the FGFR3 signaling pathway.
- The data is compatible with epigenetic silencing of the SOCS-1 gene and constitutive activation of the JAK-STAT pathway in pituitary adenomas.
- Hypermethylation of SOCS-1 was found in about one-third of human head and neck squamous cell carcinomas tissues,SOCS-1 methylation status can differentially affect STAT3 activation
- Mutations of the tumor suppressor gene SOCS-1 in classical Hodgkin lymphoma are frequent and associated with nuclear phospho-STAT5 accumulation
- The STAT1-SOCS1 pathway regulates the innate immune response via TLR3 signaling in epidermal keratinocytes.
- These results in our study indicates gene silencing of SOCS1 remarkably enhanced the cytotoxicity efficiency of CML28 DNA vaccine in DCs.
- The increase in mRNA for SOCS-1, which correlates with elevated levels of SOCS protein and positive immunostaining in M. avium/HIV-1 co-infected tissues.
- These results collectively indicate that bacterial flagellin inhibits TCR-mediated activation of T cells by inducing SOCS-1.
- elevated expression of SOCS genes is a specific lesion of breast-cancer cells that may confer resistance to proinflammatory cytokines and trophic factors, by shutting down STAT1/STAT5 signaling that mediate essential functions in the mammary gland
- SOCS1 gene might be involved in the development of adult asthma through functional genetic polymorphism
- SOCS-1 hypermethylation was seen in patients with an autoactivating JAK2 mutation & those with wild-type JAK2. Epigenetic SOCS-1 inactivation may be a complementary mechanism to the JAK2V617F mutation in the pathogenesis of myeloproliferative disorders.
- Using RT-PCR, we demonstrated for the first time that neutrophils express mRNA for SOCS-1.
- investigated 56 chronic myeloid leukemia patients and 16 controls for the methylation status of SOCS-1 gene promoter and Exon 2 regions
- All glioblastoma multiforme cell lines tested lacked SOCS1 expression.
- Increased expression of mucosal SOCS3, but not of SOCS1, may play a critical role in the development of the colonic inflammation of ulcerative colitis.
- In lymphocyte-predominant Hodgkin lymphoma SOCS1 function may thus be frequently impaired by mutations, and this may contribute to high JAK2 expression and activation of the JAK2/STAT6 pathway.
- mediastinal B-cell lymphoma and hodgkin lymphoma cells share overlapping features and defective tumor suppressor gene SOCS-1 triggers an oncogenic pathway operative in both Hodgkin and non-Hodgkin lymphomas.
- Together, these data demonstrate that NDRG2 expression in breast cancer cells is able to inhibit STAT3 activation via SOCS1 induction in a p38 MAPK dependent manner.
- SOCS-1 mutations qualify as a tumor suppressor in mediastinal b-cell lymphoma.
- SOCS1 is a crucial host factor that regulates the intracellular dynamism of HIV-1 Gag
- distribution of SOCS-1 in the liver tissue of chronic hepatitis B is variable
- SOCS1 and SOCS3 critically regulate influenza A virus-triggered innate immune responses by inhibiting type I interferon receptor (IFNAR)1 antiviral signaling and modulating inflammatory signaling pathways.
- SOCS1 might act as a suppressor for pulmonary fibrosis. SOCS1 might be a target of idiopathic pulmonary fibrosis treatment.
- The methylation status of CpG islands of SOCS1 genes in chronic myeloproliferative neoplasms.
- the lymphadenitis due to M. tuberculosis was associated with activated lysozymes and SOCS-3 but not SOCS-1 compared to controls, which may play a role in the long-term bacterial replication and altered immune modulation characteristic of the disease.
- Oncolytic herpes simplex virus-mediated upregulation of SOCS1 correlated with sensitivity to virus, and depletion of SOCS1 impaired virus replication by >10-fold.
- We hypothesize that SOCS1 functions as suppressor of IFN-gamma signaling, not only by inhibiting STAT1 activation but also by sustaining ERK1/2-dependent antiinflammatory pathways.
- present study suggests that SOCS-1 methylation in hepatocellular carcinoma may be negatively associated with HB(s)Ag status
- lymphocyte SOCS1 correlated with TNFalpha, pulse wave velocity and systolic blood pressure
- The results identify a hitherto unknown transport of SOCS1 into the nucleus which extends the spectrum of SOCS1 inhibitory activity.
- These data suggest that SOCS-1 inhibits high glucose-induced overexpression of TGF-beta1 and synthesis of fibronectin in human mesangial cells, which may be via JAK/STAT pathway.
- No disease-specific CpG island methylation of SOCS1 is observed, but SOCS1 expression is raised in myeloproliferative disorder granulocytes.
- difference in SOCS1, SOCS2 and SOCS3 transcript levels between normal individuals and SLE patients is not statistically significant
- CCL11 induces SOCS1 and SOCS3 expression in murine macrophages, human monocytes, and dendritic cells and inhibits GM-CSF-mediated STAT5 activation and IL-4-induced STAT6 activation in a range of hematopoietic cells.
- SOCS1-regulation of the IFN beta-dependent component of the LPS-induced TLR4 signaling pathway may contribute to the down-regulation of inflammatory cytokine production
- Data suggest that the loss of SOCS-1 expression is a critical event, leading to elevated Stat3 signaling and overexpression of MMP-2, bFGF, and VEGF, as well as enhanced invasion and angiogenesis of melanoma cells, consequently promoting brain metastasis