Browse our anti-p53 (TP53) Antibodies

Human Tumor Protein P53 (TP53) interaction partners

1. Novel insights pertaining the mechanism by which mutant p53 enhances colorectal cancer (CRC) development, which involves the expansion of cancer stem cells sub-populations within CRC tumors, and underscore the importance of targeting these sub-populations for CRC therapy.

2. A non to light smoking habit might contribute to an improvement in prognosis that is equivalent to that of wild-type KRAS, and p53 mutation did not affect survival in smokers harboring KRAS codon 12.

3. the MEG3-P53 pathway is involved in the apoptosis of A549cells induced by Paclitaxel

4. HBx levels are upregulated via a positive feedback loop involving p53 and PA28gamma to stimulate hepatitis B virus propagation.

5. Results show that P53 accumulates in the nucleus in response to AID pulses. This suggests that P53 may respond to DNA damage caused during a pulse, but P53 also enters the nucleus in response to other signals, including metabolic and oxidative stress and altered ribosome biogenesis.

6. Study reports that mutations in several cutaneous squamous cell carcinoma driver genes are present in p53 immuno-positive patches (PIPs) within normal chronically sun-exposed skin but are not detected within the non-PIP epidermis of the same skin samples. Furthermore, many of these mutations, including those in the TP53 gene, are subclonal within the PIPs.

7. Study provide evidence that TP53 and CDKN2A are the most frequently mutated genes in oral cavity squamous cell carcinoma patients.

8. Data indicate that 131 acute myeloid leukemia patients of whom 33 (25%) had a tumor protein p53 (TP53) mutation.

9. The N-terminal region is dynamically disordered in the full-length p53 tetramer, fluctuating between states in which it is free and fully exposed to solvent and states in which it makes transient contacts with the DNA-binding domain.

10. lnc-HUR1 can interact with p53 and inhibit its transcriptional regulation on downstream genes.

11. Fluctuations in the oscillatory pattern of the tumor suppressor p53 upon gamma radiation trigger a sharp switch between p21 and CDK2, leading to escape from arrest.

12. Together, HMGB1 and p53 provided a subtle balance between autophagy and apoptosis, thus determining the fate of PCB29-Polychlorinated biphenyl quinone-treated cells

13. High Rates of TP53 Mutation are associated with African American Patients with Gastric Cancer.

14. In triple-negative breast cancer patients who received adjuvant chemotherapy, immunohistochemical p53 expression was associated with better breast cancer-specific survival.

15. PAX8 positively regulates the expression of TP53 in high grade serous ovarian carcinoma (HGSC) and the pro-proliferative role of PAX8 is mediated by the gain of function activity of mutant p53. Surprisingly, mutant p53 transcriptionally activates the expression of p21, which localizes to the cytoplasm of HGSC cells where it plays a non-canonical, pro-proliferative role.

16. Ours is the first study demonstrating the association of TP53 P72R with the risk of primary angle closure glaucoma (PACG). It emphasizes that apart from narrow anterior chamber angle, impaired apoptotic mechanisms could also be an important contributor toward PACG.

17. A novel transcription-independent Gain of function mutant p53-AMPK-FOXO3a-FOXM1 signaling cascade that plays an important role in mediating mutant p53s' gain-of-function activities in Head and neck squamous cell carcinoma.

18. Dual inhibition of MDM2 and MDM4 in virus-positive Merkel cell carcinoma enhances the p53 response.

19. P53 can suppress inflammation in a plethora of human tissues. Growth Hormone - Releasing Hormone is a hypothalamic peptide with a great capacity to affect the complex networks of cellular regulation via GHRH - specific receptors. GHRH antagonistic and agonistic analogs have been developed for clinical applications

20. Restoration of 133p53 expression may be a novel therapeutic strategy to treat aging-associated phenotypes of Hutchinson-Gilford Progeria Syndrome in vivo.

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. 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.

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

3. 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

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

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

6. 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.

7. 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

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

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

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

11. 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

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

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

14. 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.

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

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

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

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

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

20. Data suggest that the co-inhibition of Tp53 activity rescued the morphological deformities but did not alleviate the erythroid aplasia indicating that ribosomal protein deficiency causes erythroid failure in a Tp53-independent manner.

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. 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.

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

3. 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.

4. 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.

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

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

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

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

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

10. we found an unanticipated effect of p53 loss in mouse and human G1-checkpoint-deficient cells: reduction of DNA damage. We show that abrogation of the G1/S-checkpoint allowed cells to enter S-phase under growth-restricting conditions at the expense of severe replication stress manifesting as decelerated DNA replication, reduced origin firing and accumulation of DNA double-strand breaks

11. indicating a general perturbation of the p53, miR-34a and SIRT1 pathway in Huntington's disease

12. Using Fanca(-/-) HSCs expressing the separation-of-function mutant p53(515C) transgene, which selectively impairs the p53 function in apoptosis but keeps its cell-cycle checkpoint activities intact, we show that the p53 cell-cycle function is specifically required for the regulation of Fanca(-/-) HSC proliferation.

13. lipid profiles are significantly altered by the lack of p53 in muscle tissues.

14. p53 becomes activated in BM endothelial cells upon hematopoietic stresses such as irradiation and chemotherapeutic treatments. The conditional activation of p53 induces the expression of p53 target genes specifically in vascular endothelial cells, resulting in the dilation and collapse of vascular endothelial cells, reductions in perivascular mesenchymal stromal cells, and depletion of HSCs.

15. p53R245W tumors are the most aggressive and exhibit metastases to lung and liver.

16. L3MBTL2 plays a protective role in kidney injury, in part by inhibiting the DNA damage-p53-apoptosis pathway.

17. results indicate that miR-148b-3p contributes to the regulation of hypoxia/reoxygenation-induced cardiomyocyte apoptosis in vitro through targeting SIRT7 and modulating p53-mediated pro-apoptotic signaling

18. Data provide evidence that p53 enhances NOXA-induced apoptosis when autophagy is inhibited.

19. The p53 is critical in activation of T lymphocytes not only by regulating proliferation and apoptosis but also because of its effective function in the pathogenesis of septic complications.

20. 133p53 promotes tumour invasion via IL-6 by activation of the JAK-STAT and RhoA-ROCK pathways.

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.