05-596
Anti-Cdk2 Antibody, clone AN4.3
clone AN4.3, Upstate®, from mouse
Synonym(e):
Anti-CDKN2, Anti-p33(CDK2)
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About This Item
UNSPSC-Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Empfohlene Produkte
Biologische Quelle
mouse
Qualitätsniveau
Antikörperform
purified antibody
Antikörper-Produkttyp
primary antibodies
Klon
AN4.3, monoclonal
Speziesreaktivität
mouse, Xenopus, human
Hersteller/Markenname
Upstate®
Methode(n)
immunoprecipitation (IP): suitable
western blot: suitable
Isotyp
IgG
NCBI-Hinterlegungsnummer
UniProt-Hinterlegungsnummer
Versandbedingung
dry ice
Posttranslationale Modifikation Target
unmodified
Angaben zum Gen
mouse ... Cdk2(12566)
Spezifität
cdk2, does not react with other cdks
Immunogen
Recombinant human cdk2
Anwendung
Research Category
Epigenetik & nukleäre Funktionen
Epigenetik & nukleäre Funktionen
Research Sub Category
Zellzyklus, DNA-Replikation & -Reparatur
Zellzyklus, DNA-Replikation & -Reparatur
0.5-2μg/ml of this lot detected cdk2 in HeLa nuclear extract. 4μg of a previous lot immunoprecipitated cdk2 from 500μg of mouse 3T3 nuclear extract.
Detect Cdk2 with Anti-Cdk2 Antibody, clone AN4.3 (Mouse Monoclonal Antibody), that has been shown to work in IP & WB.
Qualität
routinely evaluated by immunoblot on HeLa nuclear extract
Zielbeschreibung
33kDa
Physikalische Form
Protein G Chromatography
0.07M Tris-glycine, pH 7.4, 0.105M NaCl, 0.035% sodium azide, and 30% glycerol.
Format: Purified
Lagerung und Haltbarkeit
2 years at -20°C
Hinweis zur Analyse
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.
Rechtliche Hinweise
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
Haftungsausschluss
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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Lagerklassenschlüssel
10 - Combustible liquids
WGK
WGK 1
Analysenzertifikate (COA)
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K J Buchkovich et al.
Molecular biology of the cell, 7(9), 1443-1454 (1996-09-01)
Telomerase activity is involved in telomere length maintenance. Leukocytes, unlike many human somatic tissues, have detectable telomerase activity. These cells provide a normal human cell type in which to study telomerase. We studied the regulation of telomerase activity and the
Jennifer P Ditano et al.
Cell cycle (Georgetown, Tex.), 20(13), 1308-1319 (2021-06-23)
Cyclin-dependent kinase (CDK) 1 complexed with cyclin B is a driver of mitosis, while CDK2 drives S phase entry and replicon initiation. CDK2 activity increases as cells progress through S phase, and its cyclin partner switches from cyclin E to
Sara Bolin et al.
Oncogene, 37(21), 2850-2862 (2018-03-08)
Medulloblastoma (MB) is the most common malignant brain tumor in children. MYC genes are frequently amplified and correlate with poor prognosis in MB. BET bromodomains recognize acetylated lysine residues and often promote and maintain MYC transcription. Certain cyclin-dependent kinases (CDKs)
Nandini Sakurikar et al.
Oncotarget, 7(2), 1380-1394 (2015-11-26)
DNA damage activates Checkpoint kinase 1 (Chk1) to halt cell cycle progression thereby preventing further DNA replication and mitosis until the damage has been repaired. Consequently, Chk1 inhibitors have emerged as promising anticancer therapeutics in combination with DNA damaging drugs
APOLLON protein promotes early mitotic CYCLIN A degradation independent of the spindle assembly checkpoint.
Kikuchi, R; Ohata, H; Ohoka, N; Kawabata, A; Naito, M
The Journal of Biological Chemistry null
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