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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.


hRad54, RAD54L
The protein encoded by this gene belongs to the DEAD-like helicase superfamily, and shares similarity with Saccharomyces cerevisiae Rad54, a protein known to be involved in the homologous recombination and repair of DNA. This protein has been shown to play a role in homologous recombination related repair of DNA double-strand breaks. The binding of this protein to double-strand DNA induces a DNA topological change, which is thought to facilitate homologous DNA paring, and stimulate DNA recombination. Alternative splicing results in multiple transcript variants encoding the same protein.[provided by RefSeq, Dec 2008] (from NCBI)
Top mentioned proteins: Rad51, RAD54, CAN, BRG1, TID1
Papers on hRad54
The p53-p21-DREAM-CDE/CHR pathway regulates G2/M cell cycle genes.
Engeland et al., Leipzig, Germany. In Nucleic Acids Res, Feb 2016
The target gene list was verified by detailed analysis of p53-dependent repression of the cell cycle genes B-MYB (MYBL2), BUB1, CCNA2, CCNB1, CHEK2, MELK, POLD1, RAD18 and RAD54L.
Genetic variations in the homologous recombination repair pathway genes modify risk of glioma.
Zhou et al., Shanghai, China. In J Neurooncol, Jan 2016
P = 0.001), and RAD54L rs1048771 (OR 1.61, 95 % CI 1.17-2.22,
Impact of Polymorphic Variations of Gemcitabine Metabolism, DNA Damage Repair, and Drug Resistance Genes on the Effect of High-Dose Chemotherapy for Relapsed or Refractory Lymphoid Malignancies.
Nieto et al., Houston, United States. In Biol Blood Marrow Transplant, Jan 2016
EXPERIMENTAL DESIGN: We evaluated 21 germline SNPs of the gemcitabine metabolism genes CDA, dCK, and hCNT3, DNA damage repair genes RECQL, XRCC1, RAD54L, ATM, ATR, MLH1, MSH2, MSH3, TREX1, EXO1, and TP73, and multidrug resistance genes MRP2 and MRP5, as well as glutathione-S-transferase GSTP1 in 153 patients with relapsed or refractory lymphoma or myeloma receiving Gem/Bu/Mel.
MicroRNA-Related DNA Repair/Cell-Cycle Genes Independently Associated With Relapse After Radiation Therapy for Early Breast Cancer.
Molloy et al., Australia. In Int J Radiat Oncol Biol Phys, Jan 2016
The expression of putative microRNA target biomarkers-TOP2A, POLQ, RAD54L, SKP2, PLK2, and RAG1-were correlated with standard clinicopathologic variables using 2-sided nonparametric tests, and to local/distant relapse and survival using Kaplan-Meier and Cox regression analysis.
Interactions of DNA repair gene variants modulate chromosomal aberrations in healthy subjects.
Hemminki et al., Heidelberg, Germany. In Carcinogenesis, Nov 2015
A significant association of heterozygous variant genotype in RAD54L with increased CSA frequency (OR 1.96, 95% CI 1.01-4.02,
Concurrent Gain of Oncogenes Drives Choroid Plexus Carcinoma.
In Cancer Discov, Jul 2015
TAF12, NFYC, and RAD54L are oncogenes required to initiate and maintain choroid plexus carcinoma (CPC).
Cell cycle regulation of human DNA repair and chromatin remodeling genes.
Krokan et al., Trondheim, Norway. In Dna Repair (amst), Jun 2015
genes for chromatin assembly factor 1 (CAF-1) major subunits CHAF1A and CHAF1B; the putative helicases HELLS and ATAD2 that both co-activate E2F transcription factors central in G1/S-transition and recruit DNA repair and chromatin-modifying proteins and DNA double strand break repair proteins; and RAD54L and RAD54B involved in double strand break repair.
Cross-Species Genomics Identifies TAF12, NFYC, and RAD54L as Choroid Plexus Carcinoma Oncogenes.
Gilbertson et al., Memphis, United States. In Cancer Cell, Jun 2015
TAF12, NFYC, and RAD54L co-located on human chromosome 1p32-35.3
RAD54 family translocases counter genotoxic effects of RAD51 in human tumor cells.
Bishop et al., Chicago, United States. In Nucleic Acids Res, May 2015
We further show that combined depletion of RAD54L and RAD54B and/or artificial induction of RAD51 overexpression blocks replication and promotes chromosome segregation defects.
Germline TYMS genotype is highly predictive in patients with metastatic gastrointestinal malignancies receiving capecitabine-based chemotherapy.
Schellens et al., Sankt Gallen, Switzerland. In Cancer Chemother Pharmacol, Apr 2015
METHODS: We assessed 44 gene polymorphisms in 16 genes (TYMS, MTHFR, GSTP1, GSTM1, GSTT1, DPYD, XRCC1, XRCC3, XPD, ERCC1, RECQ1, RAD54L, ABCB1, ABCC2, ABCG2 and UGT2B7) in 64 patients with metastatic colorectal cancer (CRC) receiving capecitabine/oxaliplatin and 76 patients with advanced gastroesophageal cancer (GEC) receiving epirubicin/cisplatin/capecitabine, respectively.
Gene expression changes in residual advanced cervical cancer after radiotherapy: indicators of poor prognosis and radioresistance?
Cai et al., Fuzhou, China. In Med Sci Monit, 2014
High differential expression of CXCL12, CD74, FGF7, COL14A1, PRC1, and RAD54L genes was validated by quantitative PCR before and after radiotherapy.
The RAD51-stimulatory compound RS-1 can exploit the RAD51 overexpression that exists in cancer cells and tumors.
Connell et al., Chicago, United States. In Cancer Res, 2014
Resistance to RS-1 tended to occur in cells with higher levels of RAD54L and RAD54B, which are Swi2/Snf2-related translocases known to dissociate RAD51 filaments from dsDNA.
Promoter CpG island methylation of genes in key cancer pathways associates with clinical outcome in high-grade serous ovarian cancer.
Brown et al., Glasgow, United Kingdom. In Clin Cancer Res, 2013
Of 17 out of the 28 genes represented in the TCGA data set, methylation of VEGFB, VEGFA, HDAC11, FANCA, E2F1, GPX4, PRDX2, RAD54L, and RECQL4 was prognostic in this independent patient cohort (one-sided P < 0.05, false discovery rate < 10%).
Rad51 protein stimulates the branch migration activity of Rad54 protein.
Mazin et al., Philadelphia, United States. In J Biol Chem, 2008
Rad51 protein stimulates the branch migration activity of Rad54 protein.(
Germline mutations in RAD51, RAD51AP1, RAD51B, RAD51C,RAD51D, RAD52 and RAD54L do not contribute to familial chronic lymphocytic leukemia.
Houlston et al., United Kingdom. In Leuk Lymphoma, 2008
germline mutations in RAD51, RAD51AP1, RAD51L1, RAD51L3, RAD52 and RAD54L are unlikely to be causal of an inherited predisposition to CLL.
Rad54 dissociates homologous recombination intermediates by branch migration.
Mazin et al., Philadelphia, United States. In Nat Struct Mol Biol, 2007
Rad54 protein causes dissociation of joint molecules by ATP-dependent branch-migration and therefore plays an important role in double strand DNA break repair.
Interactions of human rad54 protein with branched DNA molecules.
Mazin et al., Philadelphia, United States. In J Biol Chem, 2007
analysis of human rad54 protein interactions with branched DNA molecules
Homology-driven chromatin remodeling by human RAD54.
Kingston et al., Boston, United States. In Nat Struct Mol Biol, 2007
RAD54 is recruited by RAD51-ssDNA filament to the chromatin of the intact chromosome and it remodels that chromatin to facilitate accessibility for strand exchange
Single nucleotide polymorphisms of RecQ1, RAD54L, and ATM genes are associated with reduced survival of pancreatic cancer.
Abbruzzese et al., Houston, United States. In J Clin Oncol, 2006
RESULTS: The RecQ1 A159C, RAD54L C157T, XRCC1 R194W, and ATM T77C genotypes had a significant effect on the overall survival with log-rank P values of .001,
Mechanisms underlying targeted gene correction using chimeric RNA/DNA and single-stranded DNA oligonucleotides.
Jensen et al., Århus, Denmark. In J Mol Med (berl), 2002
Protein factors such as hRad52, hRad54, hRPA, and p53 may modulate the heteroduplex formation and participate in the activation of the endogenous mismatch repair and/or nucleotide excision repair pathway(s).
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