05-655
Anti-p21/WAF1/Cip1 Antibody, clone CP74
clone CP74, Upstate®, from mouse
Synonym(s):
Anti-CAP20, Anti-CIP1, Anti-MDA-6, Anti-P21, Anti-SDI1, Anti-WAF1, Anti-p21CIP1
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All Photos(2)
About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
antibody form
purified antibody
antibody product type
primary antibodies
clone
CP74, monoclonal
species reactivity
human
manufacturer/tradename
Upstate®
technique(s)
immunohistochemistry: suitable
western blot: suitable
isotype
IgG2bκ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... CDKN1A(1026)
Specificity
Cip1
Immunogen
Recombinant full-length human Cip1 with an N-terminal histidine tag; epitope corresponds to amino acids 1-80 of full-length human Cip1
Application
Anti-p21/WAF1/Cip1 Antibody, clone CP74 is a high quality Mouse Monoclonal Antibody for the detection of p21/WAF1/Cip1 & has been validated in WB.
Research Category
Epigenetics & Nuclear Function
Epigenetics & Nuclear Function
Research Sub Category
Cell Cycle, DNA Replication & Repair
Cell Cycle, DNA Replication & Repair
Quality
routinely evaluated by immunoblot on nuclear extract from HeLa cells
Target description
21kDa
Physical form
0.1M Tris-glycine, pH 7.4, 0.15M NaCl, 0.05% sodium azide before the addition of glycerol to 30%
Format: Purified
Protein G Purified
Storage and Stability
2 years at -20°C
Analysis Note
Control
Positive Antigen Control: Catalog #12-309, Hela cell nuclear extract. Add an equal volume of Laemmli reducing sample buffer to 10 μL of extract and boil for 5 minutes to reduce the preparation. Load 20 μg of reduced extract per lane for minigels.
Positive Antigen Control: Catalog #12-309, Hela cell nuclear extract. Add an equal volume of Laemmli reducing sample buffer to 10 μL of extract and boil for 5 minutes to reduce the preparation. Load 20 μg of reduced extract per lane for minigels.
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Product No.
Description
Pricing
Storage Class
10 - Combustible liquids
wgk_germany
WGK 1
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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STX140 and STX641 cause apoptosis via the intrinsic mitochondrial pathway and down-regulate survivin and XIAP expression in ovarian and prostate cancer cells.
Foster PA, Ho YT, Newman SP, Leese MP, Potter BV, Reed MJ, Purohit A
Anticancer research null
Z Y Yang et al.
Nature medicine, 1(10), 1052-1056 (1995-10-01)
The p21 gene encodes a cyclin-dependent kinase inhibitor that affects cell-cycle progression, but the potential of this gene product to serve as a tumour suppressor in vivo has not been established. In this report, we show that the growth of
Yongye Huang et al.
Biomedical reports, 7(1), 36-40 (2017-07-08)
Wnt signaling is critical in embryonic development and post-embryonic tissue homeostasis. The aim of the present study was to evaluate the expression levels of canonical Wnt signaling genes in porcine somatic cell nuclear transfer (SCNT) embryos. Quantitative polymerase chain reaction
N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) triggers MSH2 and Cdt2 protein-dependent degradation of the cell cycle and mismatch repair (MMR) inhibitor protein p21Waf1/Cip1.
Jascur, T; Fotedar, R; Greene, S; Hotchkiss, E; Boland, CR
The Journal of Biological Chemistry null
Expression and function of EZH2 in synovial fibroblasts: epigenetic repression of the Wnt inhibitor SFRP1 in rheumatoid arthritis.
Trenkmann M, Brock M, Gay RE, Kolling C, Speich R, Michel BA, Gay S, Huber LC
Annals of the Rheumatic Diseases null
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