Ignet

Gene Information

Gene symbol: AKT1

Gene name: v-akt murine thymoma viral oncogene homolog 1

HGNC ID: 391

Synonyms: RAC, PKB, PRKBA, AKT

Related Genes

#	Gene Symbol	Number of hits
1	CSF2	1 hits
2	EGF	1 hits
3	EIF2AK2	1 hits
4	EPHB2	1 hits
5	HLA-C	1 hits
6	HNF4A	1 hits
7	IFNG	1 hits
8	IGF1	1 hits
9	IL12A	1 hits
10	MAPK1	1 hits
11	MYC	1 hits
12	NFKB1	1 hits
13	PIK3CA	1 hits
14	PRKCA	1 hits
15	RNF213	1 hits
16	STAT3	1 hits
17	TBX21	1 hits
18	TP53	1 hits

Related Sentences

#	PMID	Sentence
1	28936833	The top 10 important nodes of SAP overlapped with Salvianolate injection and aspirin included MAPK14, MAPK8, IL-6 and IL-8.
2	28936833	The important SAP nodes overlapped with Salvianolate injection alone included AKT1 and IFNG, and the important SAP nodes overlapped with aspirin included EPHB2 and TP53.
3	28714020	Transcription factor NFKB1 may activate miR‑146b and AKT may activate miR‑21.
4	28714020	In addition, miR‑21 had a regulatory effect on IFNG expression and miR‑146b may regulate the expression of BCL2, PTEN and IFNG.
5	28714020	Furthermore, target genes of miR‑146b and miR‑21 were significantly enriched in 14 Gene Ontology terms including regulation of cell proliferation (e.g., BCL2, PTEN and IFNG).
6	28714020	Furthermore, miR‑146b may be activated by NFKB1 and subsequently reduce the expression of BCL2, PTEN and IFNG in the progression of renal fibrosis.
7	28235773	TLR10 engagement affects both the MAPK and Akt signaling pathways, leading to changes in the transcriptome of isolated human monocytes.
8	27053161	Th2 cells produce Th2 cytokines such as IL-4, IL-5 and IL-13, but repress Th1 cytokine IFNγ.
9	27053161	We herein show that phosphorylation of Gata3 at Ser308, Thr315 and Ser316 induces dissociation of a histone deacetylase Hdac2 from the Gata3/Chd4 repressive complex in Th2 cells.
10	27053161	We also identify Akt1 as a Gata3-phosphorylating kinase, and the activation of Akt1 induces derepression of Tbx21 and Ifng expression in Th2 cells.
11	26278786	We herein report that pro-inflammatory cytokines, IFNG and TNFA, synergistically activated transcription of RNF213 both in vitro and in vivo.
12	26278786	We herein report that pro-inflammatory cytokines, IFNG and TNFA, synergistically activated transcription of RNF213 both in vitro and in vivo.
13	26278786	Using various chemical inhibitors, we found that AKT and PKR pathways contributed to the transcriptional activation of RNF213.
14	26278786	Using various chemical inhibitors, we found that AKT and PKR pathways contributed to the transcriptional activation of RNF213.
15	26278786	Chemical inhibitors for AKT (LY294002) and PKR (C16) disrupted their angiogenic potentials, suggesting that RNF213 and its upstream pathways cooperatively organize the process of angiogenesis.
16	26278786	Chemical inhibitors for AKT (LY294002) and PKR (C16) disrupted their angiogenic potentials, suggesting that RNF213 and its upstream pathways cooperatively organize the process of angiogenesis.
17	24012778	In addition, primary porcine trophectoderm (pTr) cells treated with EGF exhibited increased abundance of phosphorylated (p)-AKT1, p-ERK1/2 MAPK and p-P90RSK over basal levels within 5min, and effect that was maintained to between 30 and 120min.
18	24012778	Immunofluorescence microscopy revealed abundant amounts of p-ERK1/2 MAPK and p-AKT1 proteins in the nucleus and, to a lesser extent, in the cytoplasm of pTr cells treated with EGF as compared to control cells.
19	24012778	Furthermore, the abundance of p-AKT1 and p-ERK1/2 MAPK proteins was inhibited in control and EGF-treated pTr cells transfected with EGFR siRNA.
20	24012778	Compared to the control siRNA transfected pTr cells, pTr cells transfected with EGFR siRNA exhibited an increase in expression of IFND and TGFB1, but there was no effect of expression of IFNG.
21	24012778	Further, EGF stimulated proliferation and migration of pTr cells through activation of the PI3K-AKT1 and ERK1/2 MAPK-P90RSK cell signaling pathways.
22	23668260	The infected mice displayed a significant up-regulation in the expression of chemokines (Cxcl1, Cxcl2 and Ccl2), numerous pro-inflammatory cytokines (Ifng, Il1b, Il6, and Il17f), as well as Il22 and a number of anti-microbial peptides (Defa1, Defa28, Defb1, Slpi and Reg3g) at the site(s) of infection.
23	23668260	However, CD4 T cells of the untreated and C. difficile-infected mice expressed similar levels of CD69 and CD25.
24	23668260	Neither tissue had up-regulated levels of Tbx21, Gata3 or Rorc.
25	23668260	They also displayed significantly higher phosphorylation of AKT and signal transducer and activator of transcription 3 (STAT3), an indication of pro-survival signalling.
26	23668260	These data underscore the local, innate, pro-inflammatory nature of the response to C. difficile and highlight eIF2α phosphorylation and the interleukin-22-pSTAT3-RegIIIγ axis as two of the pathways that could be used to contain and counteract the damage inflicted on the intestinal epithelium.
27	23071669	These included five that were common to both ages (TNF, HNF4A, IL15, Progesterone, and YWHAZ), and others that were unique to 2 weeks (e.g.
28	23071669	These included five that were common to both ages (TNF, HNF4A, IL15, Progesterone, and YWHAZ), and others that were unique to 2 weeks (e.g.
29	23071669	MYC/MYCN, TGFB1, and IL2) and to 4 weeks (e.g.
30	23071669	MYC/MYCN, TGFB1, and IL2) and to 4 weeks (e.g.
31	23071669	IFNG, beta-estradiol, p53, NFKB, AKT, PRKCA, IL12, and HLA-C).
32	23071669	IFNG, beta-estradiol, p53, NFKB, AKT, PRKCA, IL12, and HLA-C).
33	23071669	Based on the literature, genes that may play a role in regulating metabolic pathways at 2 weeks include Myc and HNF4A, and at 4 weeks, beta-estradiol, p53, Akt, HNF4A and AR.
34	23071669	Based on the literature, genes that may play a role in regulating metabolic pathways at 2 weeks include Myc and HNF4A, and at 4 weeks, beta-estradiol, p53, Akt, HNF4A and AR.
35	18653623	Insulin-like growth factor-1 delays Fas-mediated apoptosis in human neutrophils through the phosphatidylinositol-3 kinase pathway.
36	18653623	We previously showed that insulin-like growth factor-1 (IGF1) delays spontaneous neutrophil apoptosis without influencing the secretion of cytokines by these cells.
37	18653623	We show that IGF1 delays neutrophil apoptosis triggered by the agonistic anti-Fas antibody CH11 and that the effect of IGF1 is comparable in magnitude to that of the acknowledged anti-apoptotic cytokines interferon-gamma (IFNG) and granulocyte-macrophage colony-stimulating factor (GM-CSF; now known as CSF2).
38	18653623	IGF1 did not affect Fas expression or activation by anti-Fas of caspase-8, but inhibited the depolarization of the mitochondrial membrane.
39	18653623	Inhibitor studies indicate that the phosphatidylinositol-3 kinase (PI3K) pathway, but not the MEK-ERK pathway, mediates the effects of IGF1.
40	18653623	However, in contrast to CSF2, IGF1 did not induce phosphorylation and translocation to the membrane of AKT, the canonical downstream target of PI3K.
41	18653623	We therefore speculate that other downstream targets of PI3K are involved in the delay of neutrophil apoptosis by IGF1, possibly through stabilization of the mitochondrial membrane.