MAB3775
Anti-Cdc20 Antibody, clone AR12
clone AR12, Chemicon®, from mouse
Sinónimos:
Cell Division Cycle Protein 20 Homolog, p55cdc
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About This Item
Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Productos recomendados
origen biológico
mouse
Nivel de calidad
forma del anticuerpo
purified immunoglobulin
tipo de anticuerpo
primary antibodies
clon
AR12, monoclonal
reactividad de especies
human
fabricante / nombre comercial
Chemicon®
técnicas
immunofluorescence: suitable
immunoprecipitation (IP): suitable
isotipo
IgG1
Nº de acceso NCBI
Nº de acceso UniProt
Condiciones de envío
wet ice
modificación del objetivo postraduccional
unmodified
Información sobre el gen
human ... CDC20(991)
Especificidad
Recognizes human Cdc20
Inmunógeno
Human Cdc20 recombinant protein
Aplicación
Anti-Cdc20 Antibody, clone AR12 is a Mouse Monoclonal Antibody for detection of Cdc20 also known as Cell Division Cycle Protein 20 Homolog p55cdc & has been validated in IF & IP.
Immunofluorescence
Immunoprecipitation
Optimal working dilutions must be determined by end user.
Immunoprecipitation
Optimal working dilutions must be determined by end user.
Research Category
Epigenetics & Nuclear Function
Epigenetics & Nuclear Function
Research Sub Category
Cell Cycle, DNA Replication & Repair
Cell Cycle, DNA Replication & Repair
Forma física
Format: Purified
Purified immunoglobulin. Liquid in 0.02M phosphate buffer, 0.25M NaCl, pH 7.6, with 0.1% sodium azide.
Almacenamiento y estabilidad
Maintain at 2-8°C in undiluted aliquots for up to 12 months from date of receipt.
Información legal
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
Cláusula de descargo de responsabilidad
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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Código de clase de almacenamiento
10 - Combustible liquids
Clase de riesgo para el agua (WGK)
WGK 2
Punto de inflamabilidad (°F)
Not applicable
Punto de inflamabilidad (°C)
Not applicable
Certificados de análisis (COA)
Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»
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James Bancroft et al.
Molecular biology of the cell, 31(21), 2315-2330 (2020-08-07)
Ubiquitin-dependent proteolysis of cyclin B and securin initiates sister chromatid segregation and anaphase. The anaphase-promoting complex/cyclosome and its coactivator CDC20 (APC/CCDC20) form the main ubiquitin E3 ligase for these two proteins. APC/CCDC20 is regulated by CDK1-cyclin B and counteracting PP1
Mark D Gurden et al.
Oncotarget, 9(28), 19525-19542 (2016-07-18)
Accurate chromosome segregation is dependent on the spindle assembly checkpoint (SAC). In current models, the key direct role of Aurora B in the SAC has been suggested to be to promote rapid kinetochore localisation of MPS1, allowing MPS1 to generate
Jamin B Hein et al.
The Journal of cell biology, 220(5) (2021-04-06)
Tight regulation of the APC/C-Cdc20 ubiquitin ligase that targets cyclin B1 for degradation is important for mitotic fidelity. The spindle assembly checkpoint (SAC) inhibits Cdc20 through the mitotic checkpoint complex (MCC). In addition, phosphorylation of Cdc20 by cyclin B1-Cdk1 independently
Gang Zhang et al.
Nature communications, 8, 15822-15822 (2017-06-13)
Proper segregation of chromosomes depends on a functional spindle assembly checkpoint (SAC) and requires kinetochore localization of the Bub1 and Mad1/Mad2 checkpoint proteins. Several aspects of Mad1/Mad2 kinetochore recruitment in human cells are unclear and in particular the underlying direct
Naturally Occurring Mutations in the MPS1 Gene Predispose Cells to Kinase Inhibitor Drug Resistance.
Mark D Gurden et al.
Cancer research, 75(16), 3340-3354 (2015-07-24)
Acquired resistance to therapy is perhaps the greatest challenge to effective clinical management of cancer. With several inhibitors of the mitotic checkpoint kinase MPS1 in preclinical development, we sought to investigate how resistance against these inhibitors may arise so that
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