Modulation of signal transducers and activators of transcription (STAT) factor pathways during focal cerebral ischaemia: a gene expression array study in rat hippocampus after middle cerebral artery occlusion.
Using human brain samples from the temporal cortex from ND and AD cases, SOCS-1 through SOCS-7 and CIS mRNA and SOCS-1 through SOCS-7 protein could be detected constitutively in ND and AD human brain samples.
Most interestingly, several candidate genes, including previously reported genes (BMP4, HNF4A and APOBR) and newly identified genes (SOCS4, GCH1, ATG14, RGS6, CYP7A1 and MAPK3), are involved in insulin metabolism or lipid metabolism, implicating the contribution of energy-metabolism-associated genes to the genetic basis of KET.
Additionally, in vivo experiments using a xenograft tumor mouse model revealed that TUSC7 can serve as a tumor suppressor through sponging miR-616, and upregulating SOCS4 (SOCS5) in EC.
Clinicopathological characteristics analysis showed that SOCS4 expression was negatively associated with higher clinical stage and lymph node metastasis.
The results of the present study indicated that SOCS4 protein may be a useful regulator to inhibit cytokine overproduction, and that HSV‑SOCS4 may provide a possible solution to control cytokine storm and its consequences following induction by oncolytic virus treatment.
MicroRNA-let-7e regulates the progression and development of allergic rhinitis by targeting suppressor of cytokine signaling 4 and activating Janus kinase 1/signal transducer and activator of transcription 3 pathway.
In addition, we also demonstrated that IL-23 increases miR-25 expression levels, and overexpressed miR-25 is involved in IL-23-associated SOCS4 inhibition and cell migration and invasion.
Reduced SOCS4 level reversed the inhibitory effect of miR-1290 downregulation on cell proliferation and invasion. miR-1290 activated the JAK/STAT3 and PI3K/AKT signaling pathways by targeting SOCS4.
Hyperthermia in pigs induces suppressor of cytokine signaling (SOCS) 3 and SOCS4 expression in intestinal gut and causes disruption of inflammation cytokine production.
Furthermore, miR-1290 promoted tumor growth, invasion and metastasis <i>in vivo</i>. miR-1290 downregulated suppressor of cytokine signaling 4 (SOCS4) at both the mRNA and protein levels by targeting SOCS4.