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MAB3684

Sigma-Aldrich

Anti-Cyclin B1 Antibody, clone V152

ascites fluid, clone V152, Chemicon®

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UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

antibody form

ascites fluid

antibody product type

primary antibodies

clone

V152, monoclonal

species reactivity

mouse, human

manufacturer/tradename

Chemicon®

technique(s)

immunohistochemistry: suitable (paraffin)
western blot: suitable

isotype

IgG1

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... CCNB1(891)

Specificity

Cyclin B. Cyclin B1 is a marker of cell proliferation and a key component of the cell progression machinery. MAB3684 works well for detecting Cyclin B1 by Western blot and immunohistochemistry.

Immunogen

Hamster Cyclin B1.

Application

Detect Cyclin B1 with Anti-Cyclin B1 Antibody, clone V152 (Mouse Monoclonal Antibody), that has been shown to work in WB, IHC(P).
Research Category
Epigenetics & Nuclear Function
Research Sub Category
Cell Cycle, DNA Replication & Repair
Western blot

Immunohistochemistry (works on paraffin embedded tissue sections)

Optimal working dilutions must be determined by the end user.

Linkage

Replaces: 04-220

Physical form

Ascites fluid. Liquid. Contains no preservative.

Storage and Stability

Maintain at -20°C in undiluted aliquots up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles.

Legal Information

CHEMICON 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.

WGK

WGK 1

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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Martina Stagno d'Alcontres et al.
Cell cycle (Georgetown, Tex.), 13(9), 1463-1481 (2014-03-15)
Telomeres are repetitive nucleoprotein structures at the ends of chromosomes. Like most genomic regions consisting of repetitive DNA, telomeres are fragile sites prone to replication fork stalling and generation of chromosomal instability. In particular, abrogation of the TRF1 telomere binding
Roberta L Turner et al.
Journal of virology, 89(9), 5083-5096 (2015-02-20)
Infection with adenovirus triggers the cellular DNA damage response, elements of which include cell death and cell cycle arrest. Early adenoviral proteins, including the E1B-55K and E4orf3 proteins, inhibit signaling in response to DNA damage. A fraction of cells infected
Tobias Otto et al.
Proceedings of the National Academy of Sciences of the United States of America, 114(40), 10660-10665 (2017-09-20)
MicroRNAs (miRNAs) have been known to affect various biological processes by repressing expression of specific genes. Here we describe an essential function of the miR-34/449 family during differentiation of epithelial cells. We found that miR-34/449 suppresses the cell-cycle machinery in
Zhixiong Dong et al.
Journal of molecular cell biology, 10(4), 358-370 (2018-05-18)
The chromokinesin Kif4A controls proper chromosome condensation, congression/alignment, and cytokinesis to ensure faithful genetic inheritance. Here, we report that Cdk phosphorylation of human Kif4A at T1161 licenses Kif4A chromosomal localization, which, in turn, controls Kif4A early mitotic function. Phosphorylated Kif4A
Marianna Trakala et al.
Cell cycle (Georgetown, Tex.), 12(7), 1030-1041 (2013-02-23)
Aurora kinase B is a critical component of the chromosomal passenger complex, which is involved in the regulation of microtubule-kinetochore attachments and cytokinesis. By using conditional knockout cells and chemical inhibition, we show here that inactivation of Aurora B results

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