and degradation of target proteins , using specific interaction with an alternate E3 ligase component named heme-oxidised IRP2 ubiquitin ligase-1 (HOIL-1) , and as SOCS2, SOCS6 also has the ability to degrade other SOCS proteins, including SOCS7 .
Like CIS, SOCS2 is induced and regulated signalling by cytokines that activate STAT5, including IL-2 [78, 79] and shown to exert an antagonistic role in the SOCS1- and SOCS3mediated negative regulation of IL-2 and IL-3 signalling, respectively .
Increased expression of SOCS2 in malignancies like chronic myeloid leukemia (CML) [219,220] could contribute to transformation by negative interference with other SOCS molecules that normally would suppress tumor development.
example exists in solid tumours, as patients with active acromegaly and colonic polyps have shown a significantly increased SOCS2 expression, which mediated a reduction in SOCS1 expression, leading to elevated STAT5b levels, and likely leading to exaggerated GH-mediated proliferation of colonic epithelial cells .
More recent data suggest that administering probiotics can reduce H pylori induced gastritis and therefore the risk of associated gastric cancer by the increased cellular expression of SOCS2 and SOCS3 .
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