Aperçu des produits pour anti-p53 (TP53) Anticorps

Human Tumor Protein P53 (TP53) interaction partners

1. The survival advantage conferred by MCUR1-mediated mitochondrial Ca(2+) uptake was majorly caused by elevated production of mitochondrial reactive oxygen species and subsequent AKT/MDM2- induced P53 degradation.

2. TP53 p.Arg337His germline mutation prevalence in Southern Brazil: Further evidence for mutation testing in young breast cancer patients.

3. Taking these results together, it is concluded that AdCRM197 induces apoptosis of human ovarian cancer cells via the p53 pathway. Moreover, it was found that Adp53 can reverse the resistance of p53-deletion human ovarian cancer cells to AdCRM197.

4. Study shows that recessive dystrophic epidermolysis bullosa- squamous cell carcinoma (SCC) tumors harbor genetic alterations similar to those in UV-related SCCs. Mutations in NOTCH1/2/4 and TP53 and copy number alterations in MYC, together with the activation of the TGFbeta receptor signaling pathway, seem to play a major role in this malignancy.

5. he early expansion of centrosome amplification correlated with and was dependent on loss of function of the tumor suppressor p53 both through loss of wild-type expression and hotspot mutations. Our work shows that centrosome amplification in human tumorigenesis can occur before transformation, being repressed by p53.

6. molecular docking demonstrated that quercetin binds stably in the central pocket of E6, the binding site of E6AP. These data suggest that quercetin increases the nuclear localization of p53 by interrupting E6/E6AP complex formation in cervical cancer cells.

7. Brain-specific angiogenesis inhibitor 1 (BAI1) prevents proto-oncogene Protein c-mdm2 (Mdm2)-mediated tumor supressor p53 (p53) polyubiquitination, and its loss substantially reduces p53 levels.

8. The possibility of targeting mutant p53 specifically to improve clinical outcome.

9. PRIMA-1 can rescue amyloid-state p53 mutants

10. p53 protein plays a key role in the aging of melanocytes via IGF1 signaling pathways.

11. In a compairison of endometrial neoplasms to non-malignant conditions (including endometrial hyperplasia), in endometrial neoplasms, p53 is over-expressed, Bax is under-expressed and the Bcl2 to Bax ratio is higher.

12. Co-mutations in JAK and TP53 as well as MAP kinase pathway activation is associated with acute leukemia with megakaryocytic and erythroid differentiation.

13. Transfection with the BANCR expression vector significantly inhibited proliferation and promoted apoptosis of KGN cells, and significantly promoted the expression levels of proapoptotic Bax and p53. Therefore, it may be concluded that lncRNA BANCR participates in PCOS by promoting cell apoptosis through the upregulation of Bax and p53.

14. bergapten significantly increased the subG1 phase ratio to ~9% (P<0.05) in the two cell types. Further investigation demonstrated that bergapten upregulated the expression of cellular tumor antigen p53 (p53) and its downstream proteins cyclindependent kinase inhibitor 1 and cyclindependent kinase inhibitor 1B, whereas, it downregulated the expression of cyclin D1 and CDK4

15. only TP53 mutation was the strongest independent prognostic factor for overall survival for MDS patients with complex karyotype in China

16. The CTD-truncation mutations of TP53 cause IBMFS, providing important insights into the previously postulated connection between p53 and IBMFSs.

17. TP53 expression (>50% positive cells) has shorter time to treatment failure and poor overall survival independent of both the Mantle Cell Lymphoma International Prognostic Index score and Ki67 index.

18. Study identified a new mechanism that impairment of p53 K120 acetylation would affect its functional activity, leading to deficient anti-tumorigenesis function. Also, the results show that the tumorigenesis mechanism associated with the 359GG mutation is related to the creation of an aberrant splicing event, thereby depleting p53 function.

19. ERbeta modulates genistein's cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway.

20. Authors discovered a mechanistic link between inhibition of cap-dependent translation and enhanced p53 accumulation. This leads to apoptosis of cancer cells without causing collateral damage to normal cells.

Pig (Porcine) Tumor Protein P53 (TP53) interaction partners

1. Results demonstrated that p53 may mediate IFN-beta signaling to inhibit viral replication early after Transmissible gastroenteritis virus infection.

2. TGFB1 can inhibit Salmonella replication whereas TRP53 can promote Salmonella replication in porcine peripheral blood mononuclear cells and murine macrophages.

3. Inhibition of p53 signaling pathway can reverse the cell cycle arrest in G0/G1 phase induced by Porcine epidemic diarrhea virus infection.

4. in a pig model of human familial adenomatous polyposis, p53 plays a role in the early precancerous stages of polyp development

5. Knockdown of p53 led to three outcomes: 1) cell death was attenuated; 2) Tunicamycin-induced redistribution of GRP78 from the nucleus to the endoplasmic reticulum lumen was recovered; and 3) the endoplasmic reticulum-fluorescence/EGFP-calreticulin was recovered.

6. This study demonstrated that various expression levels of p53 in porcine fibroblasts could be achieved by gene targeting and RNA interference.

7. SIRT1, p53 and NF-kappaB are involved in the control of both the proliferation and the apoptosis of ovarian cells.

8. Taken together,these results demonstrated that Porcine parvovirus infection induced apoptosis in PK-15 cells through activation of p53 and mitochondria-mediated apoptosis pathway.

9. Data indicate that higher hepatic glucocorticoid receptor (GR) expression in EHL piglets attributes mainly to the enhanced transcription of GR promoter 1-9/10 from breed-specific interaction of p53 and specificity protein 1 (Sp1).

10. Taken together, these results demonstrated that transmissible gastroenteritis virus infection promoted the activation of p38 MAPK and p53 signalling, and p53 signalling might play a dominant role in the regulation of cell apoptosis.

11. role of transcription factor p53 and the metabolic hormone leptin, in controlling basic functions (proliferation, apoptosis and secretory activity) of ovarian cells

12. differential expression of p53 pathway-related genes accounts for breed-specific skeletal muscle and meat characteristics

13. CONCLUSION(S): (1) Apoptosis is involved in follicular atresia; (2) Bcl-2 is induced by warm ischemia; and (3) cryopreservation insult does not alter the apoptotic signals with short tissue preparation time.

14. Suppressive effect of FSH and LH on p53 expression and caspase-3 activity with parallel increase in bcl-2 expression and increased P production was observed.

15. p53 signaling might be a major determinant for the replicative senescence in the miniature pig fibroblast cells that have the shorter lifespan and slower growth rate compared to primary domestic pig fibroblast cells in vitro.

16. exogenous in vivo NO treatment seems to preserve VSMC from mitochondrial-dependent apoptosis and drive cells to quiescence through p53 increase

Rabbit Tumor Protein P53 (TP53) interaction partners

1. Suppressing expression of p53 was a required event in two assays of proliferative vitreoretinopathy.

2. These results suggest that p38 MAPK signal transduction pathway is critical to NO-induced chondrocyte apoptosis, and p38 plays a role by way of stimulating NF-kappaB, p53 and caspase-3 activation.

3. Our data indicate that exposure to rabbits to Pb(Ac)(2) caused a significant increase of apoptosis protein p53 and decrease in the antiapoptotic BCl2 proteins.

4. Chronically activated, monomeric PDGFRA induced prolonged activation of Akt and suppressed the level of p53.

5. In this study evidence is provided that exogenous PGF2alpha differentially modulates luteal expression of TP53 transcripts and protein depending on luteal stage.

Guinea Pig Tumor Protein P53 (TP53) interaction partners

1. P53 may play an important role in impulse noise induced-hair cell apoptosis.

Zebrafish Tumor Protein P53 (TP53) interaction partners

1. In p53/nf1-deficiencies, neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/- fish, but these fish developed various tumors that were not observed in their atrx+/+ siblings, including epithelioid sarcoma, angiosarcoma, undifferentiated pleomorphic sarcoma and rare types of carcinoma.

2. tp53 deleted zebrafish that spontaneously develop malignant peripheral nerve-sheath tumors, angiosarcomas, germ cell tumors, and an aggressive Natural Killer cell-like leukemia, were generated.

3. Nkx2.5 signaling via activation of Nkx2.5-Calr-p53 signaling pathway results in cardiac dysfunction and hyperglycemia-induced cardiomyopathy.

4. In the hsf4(null) fish, both p53 and activated-caspase3 were significantly decreased. Combined with the finding that the denucleation defect could be partially rescued through microinjection of p53, fas and bax mRNA into the mutant embryos, we directly proved that HSF4 promotes lens fiber cell differentiation by activating p53 and its downstream regulators

5. p53-target genes in Danio rerio have been identified.

6. Data indicate that genetic inhibition of autophagy promotes tumorigenesis in tumor protein p53 (tp53) mutant.

7. Data suggest that the sensitivity of p53 to expression of an editing-defective tRNA synthetase has a critical role in promoting genome integrity and organismal homeostasis.

8. Transcriptome analysis revealed that SepH deficiency induces an inflammatory response and activates the p53 pathway. Consequently, loss of seph renders larvae susceptible to oxidative stress and DNA damage. Finally, we demonstrate that seph interacts with p53 deficiency in adulthood to accelerate gastrointestinal tumor development

9. results suggest that trim69 participates in tp53-mediated apoptosis during zebrafish development.

10. mutant Mdm2 was unable to rescue a p53-induced apoptotic phenotype.

11. C/ebpalpha plays a role in liver growth regulation via the p53 pathway.

12. Results demonstrate a novel role of Klf8, achieved via modulation of p53 and met expression, in the maintenance neuronal progenitors and development of Purkinje cells and the proliferation of granule cells in the cerebella of zebrafish embryos

13. p53 has a limited role in eliciting the anemia phenotype of zebrafish models of Diamond-Blackfan anemia.

14. p53 protein accumulates during tumor formation as a result of tumor-specific inactivation of the Mdm2 pathway.

15. Delta113p53/Delta133p53 is an evolutionally conserved pro-survival factor for DNA damage stress by preventing apoptosis and promoting DNA double-strand break repair to inhibit cell senescence.

16. Apoptosis was also observed with myca expression; introduction of homozygous tp53(-/-) mutation into the myca transgenic fish reduced apoptosis and accelerated tumor progression.

17. The crystal structure of the zebrafish p53 tetramerization domain.

18. The identification of novel p53 isoforms with anti-apoptosis function generated due to alternative splicing of intron 8 of p53.

19. L-Leucine thus alleviates anaemia in RP-deficient cells in a TP53-independent manner.

20. By the loss-of-function of p53.

Cow (Bovine) Tumor Protein P53 (TP53) interaction partners

1. The effect of p53 expression on the development of cloned embryos, and its interaction with HDAC1 and DNMT3A are reported.

2. Bov-A2 insertion into the TP53 promoter in Antilopinae and Tragelaphini may not only provide a genetic network that regulates mammary involution, but can also answer the need for rapid mammary involution in Savanna antelopes

3. PI3K/Akt and p53 are redox-regulated in bovine aortic endothelial cells exposed to hydrogen peroxide

4. Results demonstrate that embryonic developmental potential is related to the time of first cleavage and that p66(shc), but not p53, is up-regulated in early arrested in vitro-produced bovine embryos.

Mouse (Murine) Tumor Protein P53 (TP53) interaction partners

1. Data suggest that tumor supressor p53 (p53) transcriptional activity was enhanced in the absence of CD44 antigen (CD44).

2. TP53 role in lymphomagenesis.

3. The p53 R72 variant increased susceptibility to mammary tumorigenesis through chronic inflammation.

4. FM0807 has anti-inflammatory activity in vitro, which suggests a potential clinical application in sepsis. The anti-inflammatory activity of FM0807 may be mediated by the ROS/JNK/p53 signaling pathway.

5. coordination of DNA repair appears to be an important process by which p53 suppresses tumor development.

6. Data suggest to reduce the risk of multiple primary cancers (MPCs) in germline tumor protein p53 (TP53) mutation carriers, radiotherapy should be avoided whenever possible, surgical treatment prioritised, and non-genotoxic treatments considered.

7. findings reveal that the CHD4/NuRD complex regulates neural differentiation of ESCs by down-regulating p53.

8. results suggest that p53 may block oncogenic transformation by decreasing BCL6 stability via caspase-1 up-regulation, whereas aberrant BCL6 expression inactivates transactivation of p53 target genes, either by inhibiting p53 acetylation by p300 or repressing TP53 gene transcription. These findings have implications for B cell development and lymphomagenesis.

9. zinc deficiency disrupts neural tube closure through decreased p53 ubiquitylation.

10. The effect of p53 on the capacity of cardiogenic transdifferentiation is evaluated using p53 wild-type (p53(+/+)), p53 heterozygous mutant (p53(+/-)), and p53 homozygous mutant (p53(-/-)) embryonic fibroblasts (MEFs). The effect of an important reprogramming factor Oct4 on cardiac transdifferentiation was also evaluated in the allelic series of p53 MEFs.

11. Mechanical cues control mutant p53 stability through a mevalonate-RhoA axis.

12. expression of multiple genes implicated in cell cycle control is altered in TFEB/TFE3 DKOs, revealing a previously unrecognized role of TFEB and TFE3 in the regulation of cell cycle checkpoints in response to stress.

13. HBV-upregulated lnc-HUR1 promotes cell proliferation and tumorigenesis by interacting with p53 to block downstream gene transcription.

14. p53 negatively regulates ischemia-induced angiogenesis and arteriogenesis. Inhibition of p53 increases ischemia-induced arteriogenesis and limb perfusion and thus represents a potential therapeutic strategy for arterial occlusive disease.

15. We found that the impaired homeostatic synaptic downscaling in Fmr1 KO neurons is caused by loss-of-function dephosphorylation of an epilepsy-associated ubiquitin E3 ligase, neural precursor cell expressed developmentally down-regulated gene 4-2, Nedd4-2. Such dephosphorylation of Nedd4-2 is surprisingly caused by abnormally stable tumor suppressor p53 and subsequently destabilized kinase Akt.

16. Distinct events induced by spinal motor neuron deficiency converge on p53 to trigger selective death of vulnerable spinal muscular atrophy motor neurons.

17. To uncover the molecular changes induced by the concurrent targeting of E-cadherin, p53, and Smad4 loss.

18. TP53 haploinsufficiency completely rescues emergency granulopoiesis in FANCC(-/-) mice.

19. P53 promotes retinoid acid-induced smooth muscle cell differentiation by targeting myocardin.

20. A tight control of p53 levels in myoblasts regulates the balance between differentiation and return to quiescence.

Xenopus laevis Tumor Protein P53 (TP53) interaction partners

1. The stabilities of the full-length p53 orthologs were marginal and correlated with the temperature of their organism, paralleling the stability of the isolated DNA-binding domains.

2. PP2A:B56{epsilon}, a substrate of caspase-3, regulates p53-dependent and p53-independent apoptosis during development.

3. Furthermore, while activities to process procaspase-8 and procaspase-9 appeared in SAMDC-overexpressed apoptotic embryos, the activity to process procaspase-8 did not appear in p53-overexpressed apoptotic embryos. [SAMDC]

4. XFDL156 actively restricts mesodermal differentiation in the presumptive ectoderm by controlling the spatiotemporal responsiveness to p53.

Horse (Equine) Tumor Protein P53 (TP53) interaction partners

1. Expression of p53 and Ki67 and presence or expression of EcPV2 and EcPV3 do not appear to be important prognosticators.

2. The allele frequency in Thoroughbred horse mares at codon 72 in exon 4 was 73.3% Arg/Pro, 17.1% Arg/Arg, 9.6% Pro/Pro. Presence of Arg/Pro was significantly associated with abortion, while Pro/Pro mares had a lower probability of abortion.

Rainbow Trout (Oncorhynchus mykiss) Tumor Protein P53 (TP53) interaction partners

1. levels of p53 in rainbow trout tissues and cell lines reported; detection of high p53 levels in gills may reflect need for elevated checkpoint readiness in a tissue that would be expected to be accessible to genotoxic compounds in the aquatic environment

Goat Tumor Protein P53 (TP53) interaction partners

1. miR-34c expression is p53-dependent in dairy goat male germline stem cells.[p53]

Medaka Tumor Protein P53 (TP53) interaction partners

1. p53 is not essential for tissue self-renewal in developing brain.

2. These results suggest that p53 positively regulates neurogenesis via cell proliferation.