p53DINP1 Antibody
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Application ![]()
| WB, E, IHC-P |
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Primary Accession | Q96A56 |
Other Accession | Q96A56, 61216823 |
Reactivity | Human, Mouse, Rat |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | IgG |
Calculated MW | 27366 Da |
Concentration (mg/ml) | 1 mg/mL |
Conjugate | Unconjugated |
Application Notes | p53DINP1 antibody can be used for detection of p53DINP1 by Western blot at 0.5 - 1 µg/mL. Antibody can also be used for immunohistochemistry starting at 2 µg/mL. |
Gene ID | 94241 |
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Other Names | p53DINP1 Antibody: SIP, Teap, p53DINP1, TP53DINP1, TP53INP1A, TP53INP1B, P53DINP1, SIP, Tumor protein p53-inducible nuclear protein 1, Stress-induced protein, tumor protein p53 inducible nuclear protein 1 |
Target/Specificity | TP53INP1; At least two isoforms of p53DINP1 are known to exist; this antibody will detect both isoforms. |
Reconstitution & Storage | p53DINP1 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. |
Precautions | p53DINP1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | TP53INP1 |
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Synonyms | P53DINP1, SIP |
Function | Antiproliferative and proapoptotic protein involved in cell stress response which acts as a dual regulator of transcription and autophagy. Acts as a positive regulator of autophagy. In response to cellular stress or activation of autophagy, relocates to autophagosomes where it interacts with autophagosome-associated proteins GABARAP, GABARAPL1/L2, MAP1LC3A/B/C and regulates autophagy. Acts as an antioxidant and plays a major role in p53/TP53-driven oxidative stress response. Possesses both a p53/TP53-independent intracellular reactive oxygen species (ROS) regulatory function and a p53/TP53-dependent transcription regulatory function. Positively regulates p53/TP53 and p73/TP73 and stimulates their capacity to induce apoptosis and regulate cell cycle. In response to double-strand DNA breaks, promotes p53/TP53 phosphorylation on 'Ser-46' and subsequent apoptosis. Acts as a tumor suppressor by inducing cell death by an autophagy and caspase-dependent mechanism. Can reduce cell migration by regulating the expression of SPARC. |
Cellular Location | Cytoplasm, cytosol. Nucleus. Nucleus, PML body. Cytoplasmic vesicle, autophagosome. Note=Shuttles between the nucleus and the cytoplasm, depending on cellular stress conditions, and re- localizes to autophagosomes on autophagy activation |
Tissue Location | Ubiquitously expressed. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
p53DINP1 Antibody: Apoptosis is related to many diseases and development. The p53 tumor-suppressor protein induces apoptosis through transcriptional activation of several genes. A novel p53 inducible gene was identified recently and designated p53DINP1 (for p53-dependent damage-inducible nuclear protein 1) and SIP (for stress induced protein) in human and mouse. A p53DINP1 antisense oligonucleotide inhibits and overexpression of p53DINP1 enhances Ser46 phosphorylation of p53, induction of p53AIP1, and cell death induced by DNA double-strand breaks. p53DINP1 may regulate p53-dependent apoptosis through phosphorylation at Ser46 and induction of p53AIP1. The p53DINP1/SIP gene encodes two proteins of 27 and 18 kDa in human and mouse termed p53DINP1-alpha and p53DINP1-beta or SIP27 and SIP18. p53DINP1/SIP is expressed in many tissues and induced by a variety of stress agents including UV stress, mutagenic stress, heat shock, and oxidative stress.
REFERENCES
Okamura S, Arakawa H, Tanaka T, et al. p53DINP1, a p53-inducible gene, regulates p53-dependent apoptosis. Mol. Cell. 2001; 8:85-94.
Tomasini R, Samir AA, Vaccaro MI, et al. Molecular and functional characterization of the stress-induced protein (SIP) gene and its two transcripts generated by alternative splicing. SIP induced by stress and promotes cell death. J. Biol. Chem. 2001; 276:44185-92.

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