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Human Monoclonal Tumor Protein p73 Primary Antibody for ChIP, CyTOF - ABIN4343232
Shimodaira, Yoshioka-Yamashita, Kolodner, Wang: Interaction of mismatch repair protein PMS2 and the p53-related transcription factor p73 in apoptosis response to cisplatin. in Proceedings of the National Academy of Sciences of the United States of America 2003
Show all 49 Pubmed References
Human Monoclonal Tumor Protein p73 Primary Antibody for ChIP, ICC - ABIN252619
Costanzo, Merlo, Pediconi, Fulco, Sartorelli, Cole, Fontemaggi, Fanciulli, Schiltz, Blandino, Balsano, Levrero: DNA damage-dependent acetylation of p73 dictates the selective activation of apoptotic target genes. in Molecular cell 2002
Show all 28 Pubmed References
Human Polyclonal Tumor Protein p73 Primary Antibody for IHC (p), IP - ABIN151880
Levy, Adamovich, Reuven, Shaul: The Yes-associated protein 1 stabilizes p73 by preventing Itch-mediated ubiquitination of p73. in Cell death and differentiation 2007
Show all 13 Pubmed References
Human Monoclonal Tumor Protein p73 Primary Antibody for IP, WB - ABIN967629
Jost, Marin, Kaelin: p73 is a simian [correction of human] p53-related protein that can induce apoptosis. in Nature 1997
Show all 5 Pubmed References
Human Polyclonal Tumor Protein p73 Primary Antibody for IF (p), IHC (p) - ABIN675279
Liu, Yang, Jing, Ren, Wei, Zhang, Zhang, Duan, Zhou, Sun: Silica nanoparticle exposure inducing granulosa cell apoptosis and follicular atresia in female Balb/c mice. in Environmental science and pollution research international 2017
Human Monoclonal Tumor Protein p73 Primary Antibody for WB - ABIN252620
Shao, Tanaka, Gribi, Yu: Thioredoxin-related regulation of NO/NOS activities. in Annals of the New York Academy of Sciences 2002
Human Polyclonal Tumor Protein p73 Primary Antibody for IHC - ABIN966779
Yuan, Shioya, Ishiko, Sun, Gu, Huang, Lu, Kharbanda, Weichselbaum, Kufe: p73 is regulated by tyrosine kinase c-Abl in the apoptotic response to DNA damage. in Nature 1999
Human Monoclonal Tumor Protein p73 Primary Antibody for GS, ICC - ABIN269466
King, Reddi, Ponnamperuma, Gerdes, Weinberg: Dysregulated ΔNp63α negatively regulates the maspin promoter in keratinocytes via blocking endogenous p73 binding. in Molecular carcinogenesis 2014
DeltaNp73 was abundantly expressed in the atopic dermatitis epidermis and increased the release of TSLP (show TSLP Antibodies) via NF-kappaB (show NFKB1 Antibodies) activation.
PRIMA-1 could cause the demethylation of TP73, through DNMT1 (show DNMT1 Antibodies) depletion, to subsequently enhance the unfolded protein response
Data found that P73 G4C14-to-A4T14 polymorphism was significantly associated with non-small cell lung cancer risk in Chinese population.
In p53 (show TP53 Antibodies)-deficient breast cancers, compensatory mechanism of NFkB repression by p63 (show RPE65 Antibodies) and p73 during genotoxic stress could lead to complex effects that would influence all aspects of tumor progression.
DeltaNp73 had no leukemic transformation capacity by itself and apparently did not cooperate with the PML (show PML Antibodies)/RARA (show RARA Antibodies) fusion protein to induce a leukemic phenotype in a murine BM transplantation model.
In colorectal tumor cells RPL26 (show RPL26 Antibodies) regulates p73 expression via two distinct mechanisms: protein stability and mRNA translation.
Data show that a dominant-negative effect is widely spread within the p53 (show TP53 Antibodies)/p63 (show RPE65 Antibodies)/p73 family as all p53 (show TP53 Antibodies) loss-of-function hotspot mutants and several of the isoforms of p53 (show TP53 Antibodies) and p73 tested exhibit a dominant-negative potential.
p73 supports mitochondria respiration in medulloblastoma via regulation of glutamine (show GFPT1 Antibodies) metabolism
Study suggests that the cleavage of p73 on specific sites may release its pro-apoptotic function and contribute to cell death in breast cancer.
the transactivation inhibitory (TI) domains within the alpha-isoform-specific C termini of p63 (show RPE65 Antibodies) and p73 are essential for binding to p53R175H.
p73 is required for appropriate BMP-induced mesenchymal-to-epithelial transition during somatic cell reprogramming.
P73 (show ARHGAP24 Antibodies) role in differentiating stem cells.RASSF1A promotes a YAP (show YAP1 Antibodies)-p73 (show ARHGAP24 Antibodies) transcriptional programme that enables differentiation.
Absence of TAp73 leads to activation of TGF-beta (show TGFB1 Antibodies) signaling through a Sma (show ACTA2 Antibodies) and Mad-related proteins-independent pathway, favoring oncogenic transforming growth factor-beta effects and epithelial-to-mesenchymal transition.
Findings reinforce the role of TAp73 as tumor suppressor gene and indicate that the regulation of cellular metabolism by TAp73 contributes to its tumor suppressor function.
cells expressing both p63 (show CKAP4 Antibodies) and p73 (show ARHGAP24 Antibodies) exist in mouse epidermis and hair follicle and that hetero-tetramer complexes can be detected by immunoprecipitation in differentiating keratinocytes.
both p53 (show TP53 Antibodies) and p73 (show ARHGAP24 Antibodies) are critical in apoptosis induced by DNA damage and differentiation.
New function of p73 (show ARHGAP24 Antibodies), independent of p53 (show TP53 Antibodies), in the neurogenic architecture of the SVZ of rodent brain.
these results therefore highlight an unanticipated role for p53 (show TP53 Antibodies) family proteins in a regulatory network that integrates essential Wnt (show WNT2 Antibodies)-Tcf (show HNF4A Antibodies) and nodal-Smad (show SMAD1 Antibodies) inputs.
TAp73 as necessary and sufficient for basal body docking, axonemal extension, and motility during the differentiation of Motile multiciliated cell progenitors.
p73 (show ARHGAP24 Antibodies) drives multiciliogenesis, both through transcriptional activation of a master ciliogenesis transcription factor FoxJ1 (show FOXJ1 Antibodies) and through regulation of multiple genes central to ciliogenesis.
This gene encodes a member of the p53 family of transcription factors involved in cellular responses to stress and development. It maps to a region on chromosome 1p36 that is frequently deleted in neuroblastoma and other tumors, and thought to contain multiple tumor suppressor genes. The demonstration that this gene is monoallelically expressed (likely from the maternal allele), supports the notion that it is a candidate gene for neuroblastoma. Many transcript variants resulting from alternative splicing and/or use of alternate promoters have been found for this gene, but the biological validity and the full-length nature of some variants have not been determined.
transformation related protein 73
, tumor protein p73
, tumor protein p73-like
, p53-like transcription factor
, p53-related protein