anti-SOCS5 (SOCS5) Antikörper

Human Suppressor of Cytokine Signaling 5 (SOCS5) Interaktionspartner

1. data indicated thatthe overexpression of FER1L4 promoted apoptosis and inhibited the EMT markers expression and PI3K/AKT signaling pathway activation in OS cells via downregulating miR-18a-5p to promote SOCS5.

2. Mechanistic investigations demonstrated that TUSC7 can interact with miR-616 and decrease its expression, thereby upregulating the expression of miR-616's targets SOCS4 (SOCS5).

3. Homozygous genotype of capital ES, Cyrilliccapital ES, Cyrillic gene of SOCS5 is a risk factor for allergic bronchial asthma

4. Data show that suppressor of cytokine signaling 5 (SOCS5) was differentially expressed in primary T-cell leukemia, acute (T-ALL).

5. We validated SOCS5 as a bona fide target of mir-18 and mir-25, and established, for the first time, the tumor suppressive role of SOCS5 in liver cancer

6. our data implicated that miR-132 may promote inflammation...via targeting SOCS5 in chronic obstructive pulmonary disease

7. These findings indicate that SOCS5 mediates the impaired function of dendritic cells in chronic lymphocytic leukemia patients

8. Data show that the Japanese encephalitis virus (JEV)-induced expression of miR-301a led to inhibition of the production of the transcription factor IFN regulatory factor 1 (IRF1) and the signaling protein suppressor of cytokine signaling 5 (SOCS5).

9. Here the authors show that suppressor of cytokine signaling (SOCS) five has a pivotal role in restricting influenza A virus in the airway epithelium, through the regulation of epidermal growth factor receptor (EGFR).

10. This study showed that SOCS5 expression was significantly down-regulated.

11. Opisthorchis felineus infection diminishes the risk of atopic bronchial asthma associated with the SOCS5 gene polymorphism.

12. different domains in SOCS5 contribute to two distinct mechanisms for regulation of cytokine and growth factor signaling with JAK1 and SHC-1

13. The rs6737848 SOCS5 polymorphism was significantly associated with asthma in additive model and in dominant model

14. Exogenous miR-9 effectively reduced SOCS5 levels, leading to activated JAK-STAT pathway, which promoted endothelial cell migration and tumour angiogenesis

15. Identified is a conserved region of about 70 residues in the N-terminal domains of SOCS4 and 5 that is predicted to be more ordered than the surrounding sequence.

16. The results may contribute to understanding SOCS5 and SOCS6 expression regulation in various cancer tissues, and show that these two factors may be used for diagnosing cancer.

17. Up regulation of SOCS1 and SOCS5 expression and down-regulation of SOCS3 and CIS may correlate with the development of a Th1 mediated immune response in Vogt-Koyanagi-Harada disease.

18. The reduction in EGFR levels and EGF-induced signaling in SOCS5-expressing cells requires both the Src homology-2 and SOCS box domains of SOCS5.

19. Constitutive expression of SOCS5 in transgenic mice results in reduced eosinophil infiltration in allergic conjunctivitis

Mouse (Murine) Suppressor of Cytokine Signaling 5 (SOCS5) Interaktionspartner

1. Data show that the Japanese encephalitis virus (JEV)-induced expression of miR-301a led to inhibition of the production of the transcription factor IFN regulatory factor 1 (IRF1) and the signaling protein suppressor of cytokine signaling 5 (SOCS5).

2. this study shows that DRD3 signaling evokes Socs5 expression, a negative regulator of Th2 development, which indirectly favors acquisition of Th1 phenotype

3. have identified a phosphorylation site (Ser211) within the JIR of mSOCS5 and have investigated the role of phosphorylation in modulating JAK binding using site-directed mutagenesis.

4. Identified is a conserved region of about 70 residues in the N-terminal domains of Socs4 and 5 that is predicted to be more ordered than the surrounding sequence.

5. The effect of Flt3-L on Th17 cells and expression of suppressors of cytokine signaling (SOCS) proteins in the lungs of house dust mite (HDM)-sensitized and -challenged mice, was evaluated.

6. SOCS5 regulates Th1/Th2 cell balance and suppresses IL-4

7. SOCS5-deficient CD4 T cells showed no abnormalities in Th1/Th2 differentiation and Socs5(-/-) mice showed normal resistance to infection with Leishmania major.

8. SOCS-5 associated with the EGF-R complex in an EGF-independent manner

9. Adoptive transfer of SOCS5Tg-CD4+ T cells into T- and B cell-deficient RAG-2(-/-) mice resulted in augmented leukocyte infiltration and increased peritoneal levels of IL-12, IFN-gamma, and TNF-alpha after cecal ligation and puncture