Proliferating cell nuclear antigen (PCNA), a single-copy gene, spans about 12 kb. This gene is located on human chromosome 20p13. PCNA is expressed at high levels in the thymus, bone marrow, fetal liver, and some cells of the small intestine and colon. It is located in the nucleus.
Immunogen
The epitope recognized by PLA0079 maps to a region between residues 75 and 125 of human proliferating cell nuclear antigen using the numbering given in SwissProt entry P12004 (GeneID 5111).
Application
Rabbit anti-PCNA Antibody, Affinity Purified has been used in:
Proliferating cell nuclear antigen (PCNA) protein functions as an auxiliary factor of polymerase δ. It acts as a cofactor to polymerase ε, polymerase β, and translesion synthesis polymerases, such as η, κ, λ, and θ. In chronic lymphoid leukemia (CLL) patients, intracellular levels of PCNA protein can be used as a marker to identify clinical behavior and survival.
Physical form
Tris-citrate/phosphate buffer, pH 7 to 8 containing 0.09% Sodium Azide
Other Notes
PCNA (Proliferating Cell Nuclear Antigen) was first identified as a factor expressed in the nuclei of replicating cells. PCNA plays a role in both DNA synthesis and repair. PCNA functions as a processivity factor for DNA polymerase by acting as a DNA clamp that tethers the polymerase catalytic units to the DNA template. The structure of PCNA is that of a trimeric ring that encircles and slides along replicating DNA. PCNA interacts with and is regulated by several proteins involved in cell cycle control and check point processes.
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DNA replication is a vulnerable time for genome stability maintenance. Intrinsic stressors, as well as oncogenic stress, can challenge replication by fostering conflicts with transcription and stabilizing DNA:RNA hybrids. RAD18 is an E3 ubiquitin ligase for PCNA that is involved
American journal of respiratory cell and molecular biology, 54(5), 728-739 (2015-10-22)
We have reported that von Hippel-Lindau protein (pVHL) expression is elevated in human and mouse fibrotic lungs and that overexpression of pVHL stimulates fibroblast proliferation. We sought to determine whether loss of pVHL in fibroblasts prevents injury and fibrosis in
PCNA on the crossroad of cancer
Stoimenov I, Helleday T
Atlas of Genetics and Cytogenetics in Oncology and Haematology (2009)
Ectopic R-loop accumulation causes DNA replication stress and genome instability. To avoid these outcomes, cells possess a range of anti-R-loop mechanisms, including RNaseH that degrades the RNA moiety in R-loops. To comprehensively identify anti-R-loop mechanisms, we performed a genome-wide trigenic
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