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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 (zeige RPE65 ELISA Kits) and p73 are essential for binding to p53R175H.
High TP73 expression is associated with glioblastoma cell invasion.
In the present study, we provide evidence that the tumor suppressor gene p73 is highly susceptible to Mn-induced neurotoxicity in the nigrostriatal system.
HECW2 is an ubiquitin ligase that stabilises p73, a crucial mediator of neurodevelopment and neurogenesis. This study implicates pathogenic genetic variants in HECW2 as potential causes of neurodevelopmental disorders in humans.
Imbalance of the apoptosis pathway, with dysregulation of p73 and TRAIL, seems to play a role in the oncogenesis of odontogenic tumors
High TP73 expression is associated with Metastasis of Hepatocellular Carcinoma.
The reduction of tumor protein p63 (zeige TP63 ELISA Kits) and tumor protein p73 isoforms, rather than alteration of DeltaN isoform expression, exerted a significant functional repercussion on cell death and proliferation in hepatitis B virus -expressing HepB cells.
p73 is epigenetically silenced in chondrosarcoma due to promoter methylation, which suggests the utility of p73 methylation as a biomarker.
A considerable number of lymphoma patients lacked the expression of either or both isoforms, while all lymphoid leukemia patients expressed both isoforms. The expression pattern differences of p73 isoforms may reflect differences in the biology of these malignancies.
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 (zeige CKAP4 ELISA Kits) and p73 (zeige ARHGAP24 ELISA Kits) exist in mouse epidermis and hair follicle and that hetero-tetramer complexes can be detected by immunoprecipitation in differentiating keratinocytes.
both p53 (zeige TP53 ELISA Kits) and p73 (zeige ARHGAP24 ELISA Kits) are critical in apoptosis induced by DNA damage and differentiation.
New function of p73 (zeige ARHGAP24 ELISA Kits), independent of p53 (zeige TP53 ELISA Kits), in the neurogenic architecture of the SVZ of rodent brain.
these results therefore highlight an unanticipated role for p53 (zeige TP53 ELISA Kits) family proteins in a regulatory network that integrates essential Wnt (zeige WNT2 ELISA Kits)-Tcf (zeige HNF4A ELISA Kits) and nodal-Smad (zeige SMAD1 ELISA Kits) inputs.
TAp73 as necessary and sufficient for basal body docking, axonemal extension, and motility during the differentiation of Motile multiciliated cell progenitors.
p73 (zeige ARHGAP24 ELISA Kits) drives multiciliogenesis, both through transcriptional activation of a master ciliogenesis transcription factor FoxJ1 (zeige FOXJ1 ELISA Kits) and through regulation of multiple genes central to ciliogenesis.
The p73 (zeige ARHGAP24 ELISA Kits) acts as a critical regulator of multiciliogenesis in its capacity as a sequence-specific transcription factor, through genomic binding and regulation of genes.
Data show that the Mdm4 (zeige MDM4 ELISA Kits)-p73 (zeige ARHGAP24 ELISA Kits) axis cannot override the dominant role of p53 (zeige TP53 ELISA Kits) in development and tumorigenesis and that Mdm4 (zeige MDM4 ELISA Kits) and p73 (zeige ARHGAP24 ELISA Kits) interaction during development and tumorigenesis suggests new insight into the role of p53 (zeige TP53 ELISA Kits) family members.
In vivo inhibition of both p63 (zeige CKAP4 ELISA Kits) and p73 (zeige ARHGAP24 ELISA Kits) in combination accelerates tumor regression and increases survival of p53 (zeige TP53 ELISA Kits)-deficient mice.
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