Aperçu des produits pour anti-p53 (TP53) Anticorps

Human Tumor Protein P53 (TP53) interaction partners

1. One of only few reports demonstrating the mutated p53 gainoffunction (GOF) activity resulting in a decrease of a malignant trait in human cancer revealed that expression of GOF mutant p53R248Q decreased the motility and invasiveness of the breast and lung cancer cells in a p53 transactivationdependent manner.

2. Results show that uniform nuclear p53 expression was associated with invasion of breast cancer tumors.

3. Among Mexican Breast cancer (BC) patients diagnosed at a young age, a high proportion with germline mutations in the TP53 gene has been identified. All patients with the TP53 mutations have a family history suggestive of Li-Fraumeni Syndrome. All patients with TP53 mutations have high-grade and HER2-positive tumors. None of these mutations or other pathological variants in TP53 are found in the healthy control group.

4. It summarizes recent evidence linking the mevalonate pathway-mutant TP53 axis with cancer progression and further discuss the clinical relevance of this axis.

5. This study is also the first to describe an IPM associated with TP53 mutations and can be used as a reference for understanding other cancers. Notably, the IPM provides an immunological perspective to elucidate the mechanisms that determine the clinical outcome of HCC.

6. malignancy and biological behavior of ovarian carcinomas depend on interaction between p-p53(Ser20) and carcinoma stem cells biomarker expression

7. This study performed extensive replica exchange with solute tempering simulations, in excess of 1.0 mus/replica, to generate disordered structural ensembles of p53-N-terminal transactivation domain (TAD) using six latest explicit solvent protein force fields. Such structural characterization is a key step toward establishing the sequence-disordered ensemble-function-disease relationship of p53.

8. P53 aberrant overexpression is frequently observed in oral cavity squamous cell carcinoma tissues as a result of point mutation or deletion[review]

9. Inactivation of HUWE1 in a human lung cancer cell line inhibited proliferation, colony-forming capacity, and tumorigenicity. Mechanistically, this phenotype was driven by increased p53, which was due to attenuated proteasomal degradation by HUWE1.

10. The tumor suppressor p53 (p53) mutant lacking the disordered C-terminal (CT) domain abolished Intersegmental transfer (IST), whereas the mutant lacking the structured core domain maintained IST, indicating the importance of the CT domain.

11. Nuclear resident HDAC4 induces senescence in human fibroblasts (BJ-TERT). HDAC4-induced senescence depends on TP53 activation.

12. the findings from our own patient cohort confirm the importance of TP53 point mutations in a subpopulation of malignant peripheral nerve sheath tumors

13. p53 expression evaluated by immunohistochemistry in bone marrow biopsy specimens at the time of AML diagnosis may indicate distinct clinical characteristics in patients with normal diploid cytogenetics and is a potentially valuable tool that can enhance risk-stratification.

14. The Meg3-dependent association of PTBP3 with the promoters of p53 target genes suggests that Meg3 and PTBP3 restrain p53 activation. Our studies reveal a novel role of Meg3 and PTBP3 in regulating p53 signaling and endothelial function, which may serve as novel targets for therapies to restore endothelial homeostasis.

15. The failure to observe stabilization of one of the mutants through the design of a second site suppressor mutation in an experimental study by our collaborators could either reflect upon the failure of the DBD (at least of this mutant) to recapitulate the complex behavior of full length p53 in the experimental construct or could result from the fact that any mutation at that conserved position is not tolerated

16. Authors found that GTSE1 could regulate the p53 function to alter the cell cycle distribution dependent on the mutation state of p53. Results reveal that GTSE1 played a key role in the progression of breast cancer

17. These results demonstrated that JSK could trigger cell cycle arrest at the G2/M phase and apoptosis in A549 and H460 cells, which was likely mediated via the p53/p21WAF1/CIP1 and p27KIP1 pathways. Overall, the results indicated that JSK may be used as an anticancer agent for the treatment of nonsmall cell lung cancer (NSCLC)

18. Low expressions of TP53 is associated with non-small cell lung cancer.

19. Mechanistic studies demonstrated that overexpression of Fn14 could reduce the formation of a Mdm2-p53-R248Q-Hsp90 complex by downregulating Hsp90 expression, indicating that degradation of p53-R248Q was accelerated via Mdm2-mediated ubiquitin-proteasomal pathway

20. P53 level and transvaginal color Doppler ultrasound can provide certain valuable clinical information for the treatment and monitoring of cervical cancer.

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. report that p53 increased in adipose tissues of 28-wk-old (aged) mice with impaired beiging capability. Cold exposure decreased p53 in beiging WAT of young mice but not in aged mice

2. the data support a tumor suppressor role for DAXX as low-dose ionizing radiation produced a higher proportion of carcinomas in Daxx heterozygous mice than wild-type controls. While DAXX has important in vivo functions, they are independent of an inhibitory role on the p53 tumor suppressor pathway.

3. these results indicate that Notch contributes to the pathogenesis of ischemic stroke by promoting p53 stability and signaling

4. that SIRT3 dysfunction leads to p53-mediated mitochondrial and neuronal damage in Alzheimer's disease

5. Study found that mouse mammary epithelium luminal progenitor cells, compared to non-clonogenic luminal cells, overexpress Trp53 and numerous p53 target genes. Loss of Trp53 induced the expansion of luminal progenitors, affecting expression of several p53 target genes. Neither p53 loss alone nor p53 loss combined with Met signaling activation caused an early detectable cell fate alteration in luminal progenitors.

6. Synthetic lethality between DNA repair factors Xlf and Paxx is rescued by inactivation of Trp53

7. These findings establish that elevated p53 activity contributes significantly to accelerated aging in Sirt6-deficient mice. The study demonstrates that p53 is a substrate of SIRT6, and highlights the importance of SIRT6-p53 axis in the regulation of aging.

8. Hypoxia-inducible factor prolyl-4-hydroxylase-1 is a convergent point in the reciprocal negative regulation of NF-kappaB and p53 signaling pathways

9. Study in mouse model finds that following Knl1 deletion, segregation errors in mitotic neural progenitor cells give rise to DNA damage on the missegregated chromosomes. This triggers rapid p53 activation and robust apoptotic and microglial phagocytic responses that extensively eliminate cells with somatic genome damage, thus causing microcephaly.

10. The authors show that activated cofilin (S3A) preferentially forms a complex with p53 and promotes its mitochondrial and nuclear localization, resulting in transcription of p53-responsive genes and promotion of apoptosis. This cofilin-p53 pro-apoptotic pathway is subject to negative regulation by PLD1 thorough cofilin inactivation and inhibition of cofilin/p53 complex formation.

11. Evolution of Tumor Formation in Humans and Mice with Inherited Mutations in the p53 Gene

12. Mitochondrial double-stranded RNA activates innate immunity in mouse cells lacking p53 protein.

13. Skeletal muscle interstitial amyloidosis occurred in 8 of 15 (53%) patients with recessive anoctaminopathy-5 in this study.

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

15. TP53 role in lymphomagenesis.

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

17. 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.

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

19. 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.

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

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.