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Ribonucleotide reductase M2 B

p53R2, RRM2B
This gene encodes the small subunit of a p53-inducible ribonucleotide reductase. This heterotetrameric enzyme catalyzes the conversion of ribonucleoside diphosphates to deoxyribonucleoside diphosphates. The product of this reaction is necessary for DNA synthesis. Mutations in this gene have been associated with autosomal recessive mitochondrial DNA depletion syndrome, autosomal dominant progressive external ophthalmoplegia-5, and mitochondrial neurogastrointestinal encephalopathy. Alternatively spliced transcript variants have been described.[provided by RefSeq, Feb 2010] (from NCBI)
Top mentioned proteins: p53, CAN, p21, HAD, POLYMERASE
Papers using p53R2 antibodies
Methemoglobinemia: from diagnosis to treatment
Usha Lydia et al., In Journal of Translational Medicine, 2007
... (1:1000, rabbit anti-human M2 antibody, Novus Biologicals [Littleton, CO]) and RNR M2b (1:1000, rabbit anti-human p53R2 antibody, Novus Biologicals) protein before (t = 0 h) and ...
Papers on p53R2
Amelioration of particulate matter-induced oxidative damage by vitamin c and quercetin in human bronchial epithelial cells.
Li et al., Taiyuan, China. In Chemosphere, Feb 2016
The results indicated that PM2.5 depleted the cell viability of 16HBE cells, elevated reactive oxygen species (ROS) generation, and inhibited mitochondrial genes expressions, including fusion proteins Mfn1 and OPA1, along with biogenesis markers SIRT1 and p53R2.
Genomic signatures for paclitaxel and gemcitabine resistance in breast cancer derived by machine learning.
Rogan et al., London, Canada. In Mol Oncol, Jan 2016
Copy number profiles of 3 genes (ABCC10, NT5C, TYMS) together with expression of 7 genes (ABCB1, ABCC10, CMPK1, DCTD, NME1, RRM1, RRM2B), predicted gemcitabine response with 85% accuracy.
Novel mutation in C10orf2 associated with multiple mtDNA deletions, chronic progressive external ophthalmoplegia and premature aging.
Thangaraj et al., Hyderābād, India. In Mitochondrion, Jan 2016
Sequencing of other nuclear genes that are associated with CPEO and multiple mtDNA deletions, such as; POLG1, POLG2, TK2, ANT1, DGUOK, MPV17 and RRM2B did not reveal any pathogenic mutation in patients with C10orf2 mutation.
PYCR1 and PYCR2 Interact and Collaborate with RRM2B to Protect Cells from Overt Oxidative Stress.
Yen et al., Duarte, United States. In Sci Rep, Dec 2015
Ribonucleotide reductase small subunit B (RRM2B) is a stress response protein that protects normal human fibroblasts from oxidative stress.
Natural products induce a G protein-mediated calcium pathway activating p53 in cancer cells.
Kenealey et al., Madison, United States. In Toxicol Appl Pharmacol, Dec 2015
Further, we demonstrate that this elevation of intracellular calcium modulates p53 activity and the subsequent transcription of several pro-apoptotic genes encoding PIG8, CD95, PIDD, TP53INP, RRM2B, Noxa, p21 and PUMA.
Ribonucleotide reductase large subunit M1 plays a different role in the invasion and metastasis of papillary thyroid carcinoma and undifferentiated thyroid carcinoma.
Shao et al., Hangzhou, China. In Tumour Biol, Nov 2015
Here, we first examined the expression level of three RR subunit proteins (RRM1, RRM2, and RRM2B) in papillary thyroid carcinoma (PTC) and undifferentiated thyroid carcinoma (UTC) patient samples by immunohistochemistry.
Expression of Ribonucleotide Reductase Subunit-2 and Thymidylate Synthase Correlates with Poor Prognosis in Patients with Resected Stages I-III Non-Small Cell Lung Cancer.
Merlo et al., Genova, Italy. In Dis Markers, 2014
The following biomarkers were investigated using IHC and q RT-PCR: excision repair cross-complementation group 1 (ERCC1), breast cancer 1 (BRCA1), ribonucleotide reductase subunits M1 and M2 (RRM1 and RRM2), subunit p53R2, thymidylate synthase (TS), and class III beta-tubulin (TUBB3).
Akt and p53R2, partners that dictate the progression and invasiveness of cancer.
Ahmadi et al., Tabrīz, Iran. In Dna Repair (amst), 2014
Furthermore, while p53R2, a p53-inducible peptide involved in the synthesis of dNTPs normally works toward suppression of cancer through elimination of reactive oxygen species (ROS), inhibition of MAPK/ERK pathway and providing dNTPs for DNA repair, the overexpression of p53R2 is reported to be associated with cancer progression and resistance to therapy.
RRM2B-Related Mitochondrial Disease
Taylor et al., Seattle, United States. In Unknown Journal, 2014
CLINICAL CHARACTERISTICS: RRM2B-related mitochondrial disease can be grouped by disease pathogenesis, phenotype, and mode of inheritance into two major types: mitochondrial DNA (mtDNA) depletion and multiple mtDNA deletions.
The roles of p53R2 in cancer progression based on the new function of mutant p53 and cytoplasmic p21.
Ahmadi et al., Tabrīz, Iran. In Life Sci, 2014
Although the deregulated expression of p53R2, a p53-inducible protein and homologue of the R2 subunit of ribonucleotide reductase, has been detected in several human cancers, p53R2 roles in cancer progression and malignancy still remains controversial.
Biomarkers for predicting the response of esophageal squamous cell carcinoma to neoadjuvant chemoradiation therapy.
Natsugoe et al., Kagoshima, Japan. In Surg Today, 2014
There are seven categories of molecules known to correlate with the response and/or prognosis: tumor suppressors (p53, p21), cell cycle regulators (Cyclin D1, CDC25B, 14-3-3sigma), DNA repair molecules (p53R2, ERCC1), drug resistance proteins [metallothionein (MT)], angiogenic factors (VEGF), molecules involved in cell proliferation/invasion/metastasis (Ki-67, COX-2) and hedgehog signaling molecules (Gli-1).
Mitochondrial depletion syndromes in children and adults.
Ahting et al., Vienna, Austria. In Can J Neurol Sci, 2013
Mutated genes phenotypically presenting with adult-onset MDS include POLG1, TK2, TyMP, RRM2B, or PEO1/twinkle.
Mammalian ribonucleotide reductase subunit p53R2 is required for mitochondrial DNA replication and DNA repair in quiescent cells.
Bianchi et al., Padova, Italy. In Proc Natl Acad Sci U S A, 2012
In nontransformed cells only during quiescence, protein p53R2 is required for maintenance of mitochondrial DNA and for optimal DNA repair after ultraviolet damage.
Expression status of ribonucleotide reductase small subunits hRRM2/p53R2 as prognostic biomarkers in stage I and II non-small cell lung cancer.
Cheng et al., T'ai-chung-shih, Taiwan. In Anticancer Res, 2011
p53R2 expression seems more important than that of hRRM2 in prognosis of early-stage lung cancer.
Gene expression analysis for predicting gemcitabine resistance in human cholangiocarcinoma.
Gotoh et al., Fukushima, Japan. In J Hepatobiliary Pancreat Sci, 2011
Increased expression of p53R2 may predict gemcitabine resistance, and upregulated RNR activity may influence gemcitabine resistance in cholangiocarcinoma cells.
Ribonucleotide reductase subunit p53R2 regulates mitochondria homeostasis and function in KB and PC-3 cancer cells.
Yen et al., Hangzhou, China. In Biochem Biophys Res Commun, 2011
this study provides functional evidence that mitochondria is one of p53R2-targeted organelles and suggests an unexpected function of p53R2, which is beyond known ribonucleotide reductase function on dNTP synthesis, in mitochondrial homeostatic control.
RRM2B mutations are frequent in familial PEO with multiple mtDNA deletions.
Taylor et al., Oxford, United Kingdom. In Neurology, 2011
Adult-onset progressive external ophthalmoplegia due to RRM2B mutations is associated with a benign myopathic phenotype and characterized by muscle-restricted, mitochondrial DNA deletions.
Mutation of RRM2B, encoding p53-controlled ribonucleotide reductase (p53R2), causes severe mitochondrial DNA depletion.
Rötig et al., Paris, France. In Nat Genet, 2007
Mutation of RRM2B is associated with mitochondrial Diseases
Impaired function of p53R2 in Rrm2b-null mice causes severe renal failure through attenuation of dNTP pools.
Arakawa et al., Tokyo, Japan. In Nat Genet, 2003
Rrm2b deficiency caused higher rates of spontaneous mutation in the kidneys of Rrm2b-/- mice. p53R2 has a pivotal role in maintaining dNTP levels for repair of DNA in resting cells.
A ribonucleotide reductase gene involved in a p53-dependent cell-cycle checkpoint for DNA damage.
Nakamura et al., Tokyo, Japan. In Nature, 2000
Here we have isolated a p53-inducible gene, p53R2, by using differential display to examine messenger RNAs in a cancer-derived human cell line carrying a highly regulated wild-type p53 expression system.
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