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Merck

OP09

Anti-p53 (Ab-2) (Pantropic) Mouse mAb (PAb1801)

liquid, clone PAb1801, Calbiochem®

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A propos de cet article

NACRES:
NA.43
UNSPSC Code:
12352203
Clone:
PAb1801, monoclonal
Species reactivity:
human
Application:
Citations:
20
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biological source

mouse

antibody form

purified antibody

antibody product type

primary antibodies

clone

PAb1801, monoclonal

form

liquid

contains

≤0.1% sodium azide as preservative

species reactivity

human

should not react with

mouse, rat

manufacturer/tradename

Calbiochem®

storage condition

do not freeze

dilution

(Frozen Sections (5 µg/mL)
Gel Shift
Immunoblotting (2.5 µg/mL)
Immunoprecipitation (1 µg/sample)
Paraffin Sections (5 µg/mL, pepsin, trypsin, or heat pre-treatment required))

isotype

IgG1

shipped in

wet ice

storage temp.

2-8°C

target post-translational modification

unmodified

Quality Level

Gene Information

human ... TP53(7157)

General description

Purified mouse monoclonal antibody generated by immunizing BALB/c mice with the specified immunogen and fusing splenocytes with SP2/0 Ag14 mouse myeloma cells (see application references). Recognizes the ~53 kDa mutant and wild-type forms of p53.
Recognizes the ~53 kDa wild-type and mutant p53 protein in A-431 cells and breast carcinoma tissue.
This Anti-p53 (Ab-2) (Pantropic) Mouse mAb (PAb1801) is validated for use in Frozen Sections, Gel Shift, Immunoblotting, IP, Paraffin Sections for the detection of p53 (Ab-2) (Pantropic).

Immunogen

Epitope: within amino acids 46-55 of human p53
Human
a human p53 fusion protein

Application

Frozen Sections (5 µg/ml)

Gel Shift (see comments)

Immunoblotting (2.5 µg/ml)

Immunoprecipitation (1 µg/sample)

Paraffin Sections (5 µg/ml, pepsin, trypsin, or heat pre-treatment required)

Packaging

Please refer to vial label for lot-specific concentration.

Physical form

In 50 mM sodium phosphate buffer, 0.2% gelatin, pH 7.5.

Analysis Note

Negative Control
SK-OV-3 cells or normal skin
Positive Control
A431 cells or breast carcinoma tissue

Other Notes

El-Deiry, W.S., et al. 1994. Cancer Res.54, 1169.
Greenblatt, M.S., et al. 1994. Cancer Res.54, 4855.
Barak, Y., et al. 1993. EMBO J.12, 461.
Kastan, M.B., et al. 1992. Cell71, 587.
Kuerbitz, S.J. 1992. Proc. Natl. Acad. Sci. USA89, 7491.
Lane, D.P. 1992. Nature358, 15.
Kastan, M.B., et al. 1991. Cancer Res.51, 6304.
Wild-type p53 has a short half-life and is present in low amounts in cells. For immunoprecipitation, increasing the amount of sample to be immunoprecipitated and applied to the gel may help visualize wild-type p53; short incubation times with 35S-Met (≤ 1 h) will help reduce background. For immunoblots of wild-type p53, maximize sensitivity by preconcentrating samples by immunoprecipitation with Cat. No. OP09, then immunoblot using Cat. No. PC35 and chemiluminescent detection. For a gel shift assay, use Cat. No. OP09L and resuspend in 100 µl buffer. Antibody should be titrated for optimal results in individual systems.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Toxicity: Standard Handling (A)

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Classe de stockage

10 - Combustible liquids

wgk

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


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Timothy Budden et al.
Oncotarget, 7(38), 60940-60953 (2016-08-04)
UVB exposure leads to DNA damage, which when unrepaired induces C>T transitions. These mutations are found throughout the melanoma genome, particularly in non-transcribed regions. The global genome repair (GGR) branch of nucleotide excision repair (NER) is responsible for repairing UV-induced
Shou-Ching Tang et al.
Breast cancer research and treatment, 84(3), 203-213 (2004-03-18)
BAG-1, a recently identified anti-apoptotic protein, is overexpressed in the majority of invasive breast carcinomas. Overexpression of BAG-1 is important for both multi-step oncogenesis and resistance of cancer cells to apoptosis induced by DNA-damaging alkylating agents. BAG-1 protein species are
James G Jackson et al.
Cancer cell, 21(6), 793-806 (2012-06-16)
Studies on the role of TP53 mutation in breast cancer response to chemotherapy are conflicting. Here, we show that, contrary to dogma, MMTV-Wnt1 mammary tumors with mutant p53 exhibited a superior clinical response compared to tumors with wild-type p53. Doxorubicin-treated
Timothy C Hallstrom et al.
Proceedings of the National Academy of Sciences of the United States of America, 100(19), 10848-10853 (2003-09-05)
Previous work has demonstrated a role for the E2F1 gene product in signaling apoptosis, both as a result of the deregulation of the Rb/E2F pathway as well as in response to DNA damage. We now show that the ability of
Roger S Jackson et al.
Cell cycle (Georgetown, Tex.), 5(24), 2889-2893 (2006-12-19)
A number of target genes for the tumor suppressor, p53, have been identified, however, the mechanisms that contribute to p53-dependent apoptosis remain to be fully elucidated. In a comprehensive screen for p53 target genes by differential display, we have identified

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