Ignet

Gene Information

Gene symbol: TP53

Gene name: tumor protein p53

HGNC ID: 11998

Synonyms: p53, LFS1

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	ATM	1 hits
3	ATR	1 hits
4	BAX	1 hits
5	BCL2	1 hits
6	BRCA1	1 hits
7	C12orf5	1 hits
8	CASP3	1 hits
9	CDKN1A	1 hits
10	CDKN2B	1 hits
11	CHEK1	1 hits
12	DDIT4	1 hits
13	FAS	1 hits
14	GAPDH	1 hits
15	GHRL	1 hits
16	GORASP1	1 hits
17	GPX1	1 hits
18	HDAC1	1 hits
19	HIST4H4	1 hits
20	HNRNPC	1 hits
21	IFNG	1 hits
22	IGF1R	1 hits
23	INS	1 hits
24	INSR	1 hits
25	KRT10	1 hits
26	MAPK1	1 hits
27	MAPK8	1 hits
28	MDM2	1 hits
29	NGF	1 hits
30	NOX4	1 hits
31	PARP1	1 hits
32	PAX3	1 hits
33	PLA2G6	1 hits
34	PLCG1	1 hits
35	PPARG	1 hits
36	PRKAA1	1 hits
37	PRKAA2	1 hits
38	RNF123	1 hits
39	SCO2	1 hits
40	SIRT1	1 hits
41	SLC2A1	1 hits
42	SOD1	1 hits
43	SOD2	1 hits
44	TNF	1 hits
45	UCP1	1 hits
46	UCP2	1 hits
47	WRN	1 hits

Related Sentences

#	PMID	Sentence
1	9398849	However, IR-induced apoptosis and Bax induction were completely normal; both of which are mediated by p53.
2	11812749	Cu/Zn-superoxide dismutase (SOD) and Mn-SOD were modestly induced, and Bcl-2 was modestly reduced; however, several other stress genes (catalase, heat shock protein 70, and p53) were unaltered.
3	11911839	This induction of Fas was not dependent upon p53, because p53 is not expressed in an active form in either HL-60 or MOLT-4 cells.
4	12947320	We characterized immunohistochemically the expression of cell cycle regulators p63, CD29, PCNA, p53, pro- and antiapoptotic proteins bcl2, bax, caspase 3 and DNA breaks, as well as keratin 10, 16 and 17.
5	14526174	WRN facilitates replication of the FXS repeat and enhances Okazaki fragment processing, thereby reducing the incidence of processes that have been suggested to lead to expansion. p53 is a protein involved in DNA damage surveillance and repair.
6	14529360	PARP(s) might regulate cell fate as essential modulators of death and survival transcriptional programs with relation to NF-kappaB and p53, proposing that inhibitors of poly(ADP-ribosyl)ation could therefore prevent the deleterious consequences of neuroinflammation by reducing NF-kappaB activity.
7	15140202	Cerebral proteasome function is reduced and ubiquitin and p53 accumulate in these brain regions, with the subsequent activation of a p53-dependent transgene and the endogenous Mdm2 gene.
8	15953818	The PARP-1 through interaction with nuclear factor-kappaB, p53, and other transcription factors might significantly modulate cell survival and death and a type of death pathway.
9	16303321	Pax3 protein is required during neural tube development to suppress p53-dependent cell death and consequent abortion of neural tube closure, but is not required to control expression of genes that direct neural tube closure.
10	16492706	This G1-phase arrest was associated with marked upregulation of the tumour suppressor p53 and the expression of cyclin-dependent kinase inhibitor p21cip1.
11	16492706	Inactivation of iPLA2 failed to arrest p53-deficient HCT cells in the G1 phase and caused massive apoptosis of p21-deficient HCT cells, suggesting that this G1-phase arrest requires activation of p53 and expression of p21cip1.
12	16492706	Furthermore, downregulation of p53 by siRNA in p21-deficient HCT cells reduced the cell death, indicating that inhibition of iPLA2 induced p53-dependent apoptosis in the absence of p21cip1.
13	16492706	Disrupting the G1-phase phospholipid turnover by inhibition of iPLA2 activates the p53-p21cip1 checkpoint mechanism, thereby blocking the entry of G1-phase cells into S phase.
14	17385193	In experimental HUVECs, we found a diminished expression of eNOS and p53, and also an enhanced expression of GLUT1 mRNA transcripts.
15	19035278	GAPDH, hnRNP D and hnRNP A/B bind specifically to the p53 CPEs and could potentially be involved in the post-transcriptional regulation of p53.
16	19806227	Sirt-1 down-regulates p53 activity, rising lifespan, and cell survival; it also deacetylases peroxisome proliferator-activated receptor-gamma (PPAR-gamma) and its coactivator 1 alpha (PGC-1alpha), promoting lipid mobilization, positively regulating insulin secretion, and increasing mitochondrial dimension and number.
17	19902175	In vitro, TNF-alpha enhanced mRNA levels of gene sets related to apoptosis and Akt and p53 but not mitochondrial or cell-cycle pathways.
18	20421300	Here, we demonstrate that the proinflammatory cytokine interleukin-1beta, combined with interferon-gamma, induces the expression of the Bcl-2 homology 3 (BH3)-only activator PUMA (p53 up-regulated modulator of apoptosis) in beta-cells.
19	20633551	The effects of HG on reduced expression of IGF-1R and increased apoptosis were blocked by silencing p53 with small interference RNA but not by non-targeting scrambled siRNA.
20	20633551	Moreover, HG negatively regulated IGF-1R promoter activity as determined by ChIP analysis, which was dependent on p53 since siRNA-p53 attenuated the effects of HG on IGF-1R promoter activity.
21	20633551	HG also increased the association of p53 with histone deacetylase 1 (HDAC1), and decreased the association of acetylated histone-4 with the IGF-1R promoter.
22	20633551	These results suggest that HG-induced repression of IGF-1R is mediated by the association of p53 with the IGF-1R promoter, and by the subsequent enhanced recruitment of chromatin-modifying proteins, such as HDAC1, to the IGF-1R promoter-p53 complex.
23	20721817	This conference report highlights selected presentations on NR2B subtype-selective NMDA receptor antagonists from Merck; selective neuronal nitric oxide synthase inhibitors from Northwestern University; novel GPR119 agonists, suchas GSK-1292263A (GlaxoSmithKline plc), PSN-821 ((OSI) Prosidion) and MBX-2982 (Metabolex Inc); a small-molecule Bcl inhibitor,navitoclax (Abbott Laboratories); and p53-targeting agents from sanofi-aventis and Ascenta Therapeutics Inc, including AT-219.
24	20861022	Inactivation of AMPK by HG up-regulated the expression and phosphorylation of p53, and p53 acted downstream of Nox4.
25	20861022	Pharmacologic activation of AMPK by 5-aminoimidazole-4-carboxamide-1-riboside in OVE26 mice attenuated Nox4 and p53 expression.
26	20861022	Our results uncover a novel function of AMPK that integrates metabolic input to Nox4 and provide new insight for activation of p53 to induce podocyte apoptosis.
27	20956556	ATM phosphorylates the p53 tumor suppressor on a site (Ser15) that regulates transcription activity.
28	20956556	This analysis demonstrates that p53 phosphorylation on an ATM site is an important mechanism in the physiological regulation of glucose homeostasis.
29	20716961	The INK4b-ARF-INK4a locus encodes for two cyclin-dependent kinase inhibitors, p15(INK4b) and p16(INK4a) and a regulator of the p53 pathway, ARF.
30	21078376	These results suggest that like diabetes, chronic depletion of Zn with TPEN induces testicular oxidative stress and damage, along with the activation of p38 MAPK and p53 signaling and mitochondria-related apoptotic cell death.
31	20586612	Null of SOD1 and GPX1 elevated respective islet superoxide and hydroperoxide production, and upregulated p53 phosphorylation.
32	20962117	Neonatal kidneys of the offspring of diabetic mothers exhibited an increased number of apoptotic cells and reactive oxygen species (ROS) generation, enhanced NF-?B activation, and nuclear translocation of its subunits (p50 and p65 subunits) as well as phosphorylation (Ser 15) of p53 compared with kidneys of offspring of nondiabetic mothers.
33	20962117	In vitro, high-glucose (25 mM) induced ROS generation and significantly increased MK4 cell apoptosis and caspase-3 activity via activation of NF-?B pathway, with p53 phosphorylation and nuclear translocation compared with normal glucose (5 mM).
34	19680556	We re-sequenced all exons, intron-exon boundaries and selected conserved non-coding sequences of candidate genes involved in aging-related processes, including dietary restriction (PPARG, PPARGC1A, SIRT1, SIRT3, UCP2, UCP3), metabolism (IGF1R, APOB, SCD), autophagy (BECN1, FRAP1), stem cell activation (NOTCH1, DLL1), tumor suppression (TP53, CDKN2A, ING1), DNA methylation (TRDMT1, DNMT3A, DNMT3B) Progeria syndromes (LMNA, ZMPSTE24, KL) and stress response (CRYAB, HSPB2).
35	20431281	SIRT1 also deacetylates a number of nonhistone target proteins, including p53, endothelial nitric oxide synthase and forkhead box protein.
36	20676904	Activation of hypertrophic and cell signaling pathways was determined by assessing protein expression levels of atrial natriuretic peptide (ANP), ?-sarcomeric actin, p53, Bax and Bcl-2 and phosphorylation of p38, ERK and Akt.
37	21185935	In vitro data indicate that cellular levels of reactive oxygen species depend on the expression and activity of p53, which plays a key role in energy metabolism and as a crucial transcription factor for SCO cytochrome oxidase deficient homolog 2 (SCO2) and tumor p53-induced glycolysis and apoptosis regulator (TIGAR), which regulate mitochondrial respiration and glycolysis in cells.
38	21185935	Exercise training decreased p53 protein levels and TIGAR expression in skeletal muscle (P<0.05), but SCO2 expression was unchanged.
39	21185935	These data indicate that exercise training can attenuate oxidative stress and increase mitochondrial DNA content in skeletal muscle in rats with T2DM and that exercise-induced suppression of p53 and TIGAR expression may play a role in preventing oxidative stress in insulin resistance.
40	20007950	On the other hand, proteins seen or predicted to be up-regulated include proteins involved in cell apoptosis (e.g. p53, 14-3-3-gamma, Serpinf1, Cct4, Cct5, and Sepina3n), proteins that neutralize the biological activity of nerve growth factor (e.g. anti-NGF 30), and proteins involved in lipid metabolism (e.g. apoA-I and apoA-IV).
41	21123956	Statins has been demonstrated to facilitate p53 degradation by activating its specific ubiquitin ligase, MDM2.
42	21123956	The p53 expression level in the ischemic limb of ATR-treated KK/Ay was significantly decreased and MDM2 phosphorylation level was markedly increased in tandem with the activation of Akt.
43	21123956	ATR was found to restore ischemic limb loss in diabetes by augmenting p53 degradation through direct activation of the Akt/MDM2 pathway in skeletal muscle.
44	21386086	Sirtuin 1 (SIRT1) is a deacetylase activated in response to calorie restriction that acts through the tumor suppressor gene p53.
45	21386086	Mice lacking p53, a target of SIRT1 action, failed to respond to ghrelin in feeding behavior.
46	21386086	Ghrelin failed to phosphorylate hypothalamic AMPK when rats were pretreated with Ex527, as it did in p53 KO mice.
47	21386086	It is noteworthy that the hypothalamic SIRT1/p53 pathway seems to be specific for mediating the orexigenic action of ghrelin, because central administration of AICAR, a potent AMPK activator, increased food intake in p53 KO mice.
48	20068143	In THP-1 cells exposed to high glucose or fatty acids in vitro, we explored SIRT1 expression, p53 acetylation, Jun NH(2)-terminal kinase (JNK) activation, NAD(+) levels, and nicotinamide phosphoribosyltransferase (NAMPT) expression.
49	20068143	High glucose and palmitate increased p53 acetylation and JNK phosphorylation; these effects were abolished in siRNA SIRT1-treated cells.
50	20222801	The activation of AMPK reprograms cellular metabolism and enforces metabolic checkpoints by acting on mTORC1, p53, fatty acid synthase and other molecules for regulating cell growth and metabolism.
51	21540236	We show that metformin increases REDD1 expression in a p53-dependent manner.
52	21776823	Receptor inhibitor studies indicated that p53 activation was mediated through insulin receptor (IR), not insulin-like growth factor-1 receptor (IGF-IR).
53	21791078	The immunocytochemical analysis and Western blotting revealed that the LDLs-induced apoptosis is associated with the activation of caspase 3 and upregulation of p53.
54	21954358	In this review, the evidence supporting the role of UCPs in diseases other than diabetes and obesity, the reports on how UCP is regulated in cancer cells, and how UCP may regulate p53 will be discussed.
55	15485917	We demonstrated that the Brca1(S971A/S971A) cells displayed reduced ability to activate the G(2)/M cell cycle checkpoint upon gamma-irradiation and to stabilize p53 following N-methyl-N'-nitro-N-nitrosoguanidine treatment.
56	16675955	Analysis of Brca1(delta11/delta11)Chk2-/- mice revealed that p53-dependent apoptosis and growth defect caused by Brca1 deficiency are significantly attenuated in rapidly proliferating organs.
57	20473325	Simultaneous deletion of one copy of p53 failed to rescue the developmental defects; however, it synergistically induced mammary tumor formation in Chk1(+/-);MMTV-Cre animals with a median time to tumor latency of about 10 months.