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Mouse Anti-TP73 Recombinant Antibody (CBYJT-4296) (CBMAB-T3776-YJ)


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Summary

Host Animal
Mouse
Specificity
Monkey
Clone
CBYJT-4296
Antibody Isotype
IgG1, κ
Application
GS, IF, IP, WB

Basic Information

Immunogen
TP73 / p73 antibody was raised against purified monkey recombinant p73alpha protein (aa380-637).
Specificity
Monkey
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Buffer
10 mM PBS, pH 7.4, 0.2% BSA
Preservative
0.09% Sodium Azide
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
aa 380-637

Target

Full Name
TP73
Introduction
TP73 functions in processes such as TP73 functions in processes such as cell cycle arrest, cellular response to UV, DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator, intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator.
Entrez Gene ID
695164
UniProt ID
F6VXE7
Function
Participates in the apoptotic response to DNA damage. Isoforms containing the transactivation domain are pro-apoptotic, isoforms lacking the domain are anti-apoptotic and block the function of p53 and transactivating p73 isoforms. May be a tumor suppressor protein. Is an activator of FOXJ1 expression (By similarity).
It is an essential factor for the positive regulation of lung ciliated cell differentiation (PubMed:34077761).
Biological Process
Biological Process cell cycle Source:UniProtKB-KW
Biological Process cellular response to DNA damage stimulus Source:UniProtKB1 Publication
Biological Process intrinsic apoptotic signaling pathway in response to DNA damage Source:ProtInc1 Publication
Biological Process intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator Source:UniProtKB2 Publications
Biological Process kidney development Source:Ensembl
Biological Process mismatch repair Source:ProtInc1 Publication
Biological Process negative regulation of cardiac muscle cell proliferation Source:MGI1 Publication
Biological Process negative regulation of cell population proliferation Source:AgBase
Biological Process negative regulation of neuron differentiation Source:Ensembl
Biological Process positive regulation of apoptotic process Source:Ensembl
Biological Process positive regulation of DNA-templated transcription Source:UniProtKB1 Publication
Biological Process positive regulation of lung ciliated cell differentiation Source:UniProtKB1 Publication
Biological Process positive regulation of MAPK cascade Source:Ensembl
Biological Process positive regulation of oligodendrocyte differentiation Source:Ensembl
Biological Process positive regulation of transcription by RNA polymerase II Source:UniProtKB3 Publications
Biological Process protein tetramerization Source:InterPro
Biological Process regulation of cell cycle Source:ParkinsonsUK-UCL1 Publication
Biological Process regulation of gene expression Source:MGI1 Publication
Biological Process regulation of mitotic cell cycle Source:MGI1 Publication
Biological Process regulation of transcription by RNA polymerase II Source:GO_Central1 Publication
Biological Process response to organonitrogen compound Source:Ensembl
Biological Process response to xenobiotic stimulus Source:Ensembl
Cellular Location
Nucleus
Cytoplasm
Accumulates in the nucleus in response to DNA damage.
Involvement in disease
Ciliary dyskinesia, primary, 47, and lissencephaly (CILD47):
A form of primary ciliary dyskinesia, a disorder characterized by abnormalities of motile cilia. Respiratory infections leading to chronic inflammation and bronchiectasis are recurrent, due to defects in the respiratory cilia. CILD47 is an autosomal recessive form characterized by onset soon after birth or in early childhood. Affected individuals also have neurologic features, such as impaired intellectual development and central hypotonia, associated with structural brain abnormalities, most notably lissencephaly and thin or absent corpus callosum. No situs abnormalities have been observed.
PTM
Isoform alpha (but not isoform beta) is sumoylated on Lys-627, which potentiates proteasomal degradation but does not affect transcriptional activity. Phosphorylation by PLK1 and PLK3 inhibits the transcription regulator activity and pro-apoptotic function.
Higher levels of phosphorylation seen in the brain from patients with Huntington disease.
Polyubiquitinated by RCHY1/PIRH2; leading to its degradation by the proteasome.
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For research use only. Not intended for any clinical use.

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