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Rabbit Anti-PMS2 Recombinant Antibody (CBYC-P478) (CBMAB-P2247-YC)

Provided herein is a Rabbit monoclonal antibody against Human PMS1 Homolog 2, Mismatch Repair System Component. The antibody can be used for immunoassay techniques, such as FC, ICC, IF, IHC-P, IP, WB.
See all PMS2 antibodies

Summary

Host Animal
Rabbit
Specificity
Human
Clone
CBYC-P478
Antibody Isotype
IgG
Application
FC, ICC, IF, IHC-P, IP, WB

Basic Information

Immunogen
A synthetic peptide corresponding to residues in human PMS2
Specificity
Human
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
50 mM Tris glycine, pH 7.4, 150 mM sodium chloride, 40% glycerol, 0.01% sodium azide and 0.05% BSA
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at-20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
PMS1 homolog 2, mismatch repair system component
Introduction
PMS2 (PMS1 Homolog 2, Mismatch Repair System Component) is a protein coding gene. Diseases associated with PMS2 include Mismatch Repair Cancer Syndrome andColorectal Cancer, Hereditary Nonpolyposis, Type 4. Among its related pathways are Gene Expression and Direct p53 effectors. Gene Ontology annotations related to this gene include ATPase activity and endonuclease activity. An important paralog of the gene is PMS1.
Entrez Gene ID
5395
UniProt ID
P54278
Alternative Names
PMS2CL; MLH4; HNPCC4; PMSL2
Function
Component of the post-replicative DNA mismatch repair system (MMR). Heterodimerizes with MLH1 to form MutL alpha. DNA repair is initiated by MutS alpha (MSH2-MSH6) or MutS beta (MSH2-MSH3) binding to a dsDNA mismatch, then MutL alpha is recruited to the heteroduplex. Assembly of the MutL-MutS-heteroduplex ternary complex in presence of RFC and PCNA is sufficient to activate endonuclease activity of PMS2. It introduces single-strand breaks near the mismatch and thus generates new entry points for the exonuclease EXO1 to degrade the strand containing the mismatch. DNA methylation would prevent cleavage and therefore assure that only the newly mutated DNA strand is going to be corrected. MutL alpha (MLH1-PMS2) interacts physically with the clamp loader subunits of DNA polymerase III, suggesting that it may play a role to recruit the DNA polymerase III to the site of the MMR. Also implicated in DNA damage signaling, a process which induces cell cycle arrest and can lead to apoptosis in case of major DNA damages.
Biological Process
Mismatch repairManual Assertion Based On ExperimentIDA:UniProtKB
Response to xenobiotic stimulusIEA:Ensembl
Somatic hypermutation of immunoglobulin genesManual Assertion Based On ExperimentIBA:GO_Central
Cellular Location
Nucleus
Involvement in disease
Hereditary non-polyposis colorectal cancer 4 (HNPCC4):
An autosomal dominant disease associated with marked increase in cancer susceptibility. It is characterized by a familial predisposition to early-onset colorectal carcinoma (CRC) and extra-colonic tumors of the gastrointestinal, urological and female reproductive tracts. HNPCC is reported to be the most common form of inherited colorectal cancer in the Western world. Clinically, HNPCC is often divided into two subgroups. Type I is characterized by hereditary predisposition to colorectal cancer, a young age of onset, and carcinoma observed in the proximal colon. Type II is characterized by increased risk for cancers in certain tissues such as the uterus, ovary, breast, stomach, small intestine, skin, and larynx in addition to the colon. Diagnosis of classical HNPCC is based on the Amsterdam criteria: 3 or more relatives affected by colorectal cancer, one a first degree relative of the other two; 2 or more generation affected; 1 or more colorectal cancers presenting before 50 years of age; exclusion of hereditary polyposis syndromes. The term 'suspected HNPCC' or 'incomplete HNPCC' can be used to describe families who do not or only partially fulfill the Amsterdam criteria, but in whom a genetic basis for colon cancer is strongly suspected.
Mismatch repair cancer syndrome 4 (MMRCS4):
An autosomal recessive form of mismatch repair cancer syndrome, a childhood cancer predisposition syndrome encompassing a broad tumor spectrum. This includes hematological malignancies, central nervous system tumors, Lynch syndrome-associated malignancies such as colorectal tumors as well as multiple intestinal polyps, embryonic tumors and rhabdomyosarcoma. Multiple cafe-au-lait macules, a feature reminiscent of neurofibromatosis type 1, are often found as first manifestation of the underlying cancer.
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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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