Publication for MCL1 and SOCS3

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	MCL1	MCL1 apoptosis regulator, BCL2 family member	4170			[link]
hsa	SOCS3	suppressor of cytokine signaling 3	9021

Pubmed ID	Priority	Text
24283803	0.97	MCL1 (lefmost panels) and SOCS3 (rightmost panels) mRNA in ML-2 cells untreated, exposed to increasing concentrations of daunorubicin (0.05 and 0.15 muM) in the absence or presence of CX-4945 5 muM (top panels) or K27 4 muM (bottom panels).
	0.83	MCL1, SOCS3 protein levels in ML-2 cells untreated, exposed to increasing concentrations of daunorubicin (0.05-0.1-0.15 muM) in the absence or presence of CX-4945 5 muM (top panels) or K27 4 muM (bottom panels).
	0.81	MCL1 and SOCS3 (Figure 7A and B) (p < 0.05, n = 3).
30302397	0.97	SOCS3 levels are inversely correlated with STAT3 phosphorylation levels via a feedback loop regulated by Janus kinases that control expression of both MCL-1 and BCL-XL.
	0.79	MCL-1 is frequently amplified in iCCAs (16-21%), and is also overexpressed via epigenetic silencing of the SOCS3 promoter by DNA hypermethylation, and upregulated by bile acids downstream of EGFR.
22403660	0.95	Mcl-1), pro-apoptotic factor (Bax), transcription factors (C/EBP-alpha, C/EBP-beta and PU.1), growth factor receptors (G-CSFR, GM-CSFR alpha, GM-CSFR beta) and suppressors of cytokine signaling (SHIP-1, SOCS1, SOCS3).
29703840	0.95	Socs3 or Mcl1, which codes for a critical anti-apoptotic protein induced by IL-15, in RId2-/- CD27+CD11b- NK cells, and we confirmed this by qRT-PCR (Fig. 2G).
25369307	0.94	SOCS-3 facilitates sustained IL-6/STAT-3 signaling with resultant enhanced Mcl-1 expression.
31222560	0.89	SOCS3, p-STAT3, c-Myc and MCL-1 was increased, decreased, increased, increased and increased, respectively.
	0.71	SOCS3 can inhibit the apoptosis of cancer cells, but the apoptosis of cancer cells increases with the inhibition of the upstream miR-221-3p. **P < 0.01 compared to the NC group; d SOCS3 inhibits the JAK/STAT signaling pathway, which is manifested in the decline in phosphorylation of STAT, as well as the decrease in the expression of c-Myc and MCL-1 in the downstream proteins, and the inhibition of SOCS3 will lead to the opposite result. And the above situation will change with the regulation of upstream miR-221-3p. **P < 0.01 compared to the NC group
23929703	0.89	SOCS3 (Table 3) and a significant decrease in STAT3, CCND1, XIAP, BIRC5 and MCL1 expression (Table 4).
25968456	0.88	SOCS3 and MCL-1 were similarly reduced in a dose-dependent manner.
28904393	0.88	SOCS3; anti-miR-18a antagonizes the inhibition effect of miR-18a, which targets PIAS3; miR-17-3p mimic augment the inhibition effect of miR-17-3p, which targets vimentin; miR-19b mimic augment the inhibition effect of miR-19b, which targets Rac and miR-20a mimic augment the inhibition effect of miR-20a, which targets Mcl1.