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Sigma-Aldrich

Anti-p16 (Ab-1) Mouse mAb (DCS-50.1/H4)

liquid, clone DCS-50.1/H4, Calbiochem®

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.43

biological source

mouse

Quality Level

antibody form

purified antibody

antibody product type

primary antibodies

clone

DCS-50.1/H4, monoclonal

form

liquid

contains

≤0.1% sodium azide as preservative

species reactivity

human

manufacturer/tradename

Calbiochem®

storage condition

do not freeze

isotype

IgG1

shipped in

wet ice

storage temp.

2-8°C

target post-translational modification

unmodified

General description

Purified mouse monoclonal antibody generated by immunizing BALB/c mice with the specified immunogen and fusing splenocytes with NS-2 mouse myeloma cells. Recognizes the ~16 kDa p16 protein.
Recognizes the ~16 kDa p16 protein in Saos-2 cells and bladder tissue. Sold under license of U.S. Patent 6,482,929. Sold under license of U.S. Patent 5,843,756, 6,090,578, and corresponding patents.
This Anti-p16 (Ab-1) Mouse mAb (DCS-50.1/H4) is validated for use in Immunoblotting for the detection of p16 (Ab-1).

Immunogen

Human
recombinant, human p16

Application

Immunoblotting (0.5-5 µg/ml, see application references)

Packaging

Please refer to vial label for lot-specific concentration.

Warning

Toxicity: Standard Handling (A)

Physical form

In 0.05 M sodium phosphate buffer, 0.2% gelatin pH 7.5.

Analysis Note

Negative Control
U2OS cells
Positive Control
Saos-2 cells or bladder tissue

Other Notes

Does not cross-react with the closely related p15 protein. Antibody should be titrated for optimal results in individual systems.
Koh, J., et al. 1995. Nature375, 506.
Lukas, J., et al. 1995. Nature375, 503.
Cheng, J.Q., et al. 1994. Cancer Res.54, 5547.
Jen, J., et al. 1994. Cancer Res.54, 6353.
Kamb, A., et al. 1994 Science264, 436.
Nobori, T., Miura, K., et al. 1994. Nature368, 753.
Okamoto, A., Demetrick, D.J., et al. 1994. Proc. Natl. Acad. Sci. USA91, 11045.
Serrano, M., et al. 1993. Nature366 704.

Legal Information

Sold under license of U.S. Patents 5,843,756, 6,090,578 and corresponding patents.
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

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Storage Class Code

10 - Combustible liquids

WGK

nwg

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Noriyasu Usami et al.
Oncogene, 22(39), 7923-7930 (2003-09-13)
We have found that a malignant mesothelioma cell line, NCI-H28, had a chromosome 3p21.3 homozygous deletion containing the beta-catenin gene (CTNNB1), which suggested that the deletion of beta-catenin might have a growth advantage in the development of this tumor. To
Goro Sashida et al.
Molecular and cellular biology, 29(13), 3687-3699 (2009-04-22)
Several ETS transcription factors, including ELF4/MEF, can function as oncogenes in murine cancer models and are overexpressed in human cancer. We found that Elf4/Mef activates Mdm2 expression; thus, lack of or knockdown of Elf4/Mef reduces Mdm2 levels in mouse embryonic
Masashi Narita et al.
Cell, 113(6), 703-716 (2003-06-18)
Cellular senescence is an extremely stable form of cell cycle arrest that limits the proliferation of damaged cells and may act as a natural barrier to cancer progression. In this study, we describe a distinct heterochromatic structure that accumulates in
Jeffrey T Irelan et al.
PloS one, 4(4), e5067-e5067 (2009-04-03)
The CDKN2A locus encodes two important tumor suppressors, INK4a and ARF, which respond to oncogenic stresses by inducing cellular senescence. We conducted a genome-scale cDNA overexpression screen using a reporter containing INK4a regulatory sequences to identify novel transcriptional activators of
J L Nargi et al.
Neoplasia (New York, N.Y.), 1(6), 544-556 (2000-08-10)
Epidemiological evidence has suggested an association between diets rich in antioxidants and diminished risks of various types of cancer. Proposed mechanisms for protective effects of antioxidants have involved inhibition of free radical-mediated DNA damage. Recent data suggest that antioxidants may

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