BRCA1 and HSP90 cooperate in homologous and non-homologous DNA double-strand-break repair and G2/M checkpoint activation.
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New treatment option for ovarian cancer: PARP inhibitorsHsp90: A New Player in DNA Repair?CHK2-BRCA1 tumor-suppressor axis restrains oncogenic Aurora-A kinase to ensure proper mitotic microtubule assembly.Hsp90 inhibitors are efficacious against Kaposi Sarcoma by enhancing the degradation of the essential viral gene LANA, of the viral co-receptor EphA2 as well as other client proteinsDifferences in the ovine HSP90AA1 gene expression rates caused by two linked polymorphisms at its promoter affect rams sperm DNA fragmentation under environmental heat stress conditionsUnderstanding the Physical and Molecular Basis of Stability of Arabidopsis DNA Pol λ under UV-B and High NaCl StressRegulation of stress-inducible phosphoprotein 1 nuclear retention by protein inhibitor of activated STAT PIAS1.Genome-wide transcriptome profiling of homologous recombination DNA repair.Histone deacetylase inhibitor treatment induces 'BRCAness' and synergistic lethality with PARP inhibitor and cisplatin against human triple negative breast cancer cellsThe breast cancer susceptibility genes (BRCA) in breast and ovarian cancers.The combination of Hsp90 inhibitor 17AAG and heavy-ion irradiation provides effective tumor control in human lung cancer cells.Identification of the interactors of human nibrin (NBN) and of its 26 kDa and 70 kDa fragments arising from the NBN 657del5 founder mutation.ARID1A Deficiency Impairs the DNA Damage Checkpoint and Sensitizes Cells to PARP InhibitorsmTOR Inhibitors Suppress Homologous Recombination Repair and Synergize with PARP Inhibitors via Regulating SUV39H1 in BRCA-Proficient Triple-Negative Breast Cancer.Toll-like receptor 8: augmentation of innate immunity in platinum resistant ovarian carcinomaReversing Platinum Resistance in High-Grade Serous Ovarian Carcinoma: Targeting BRCA and the Homologous Recombination SystemNuclear lamin stiffness is a barrier to 3D migration, but softness can limit survival.S100A2 is a BRCA1/p63 coregulated tumour suppressor gene with roles in the regulation of mutant p53 stability.Reverse the Resistance to PARP Inhibitors.Mechanisms of heat shock response in mammals.Targeting homologous recombination-mediated DNA repair in cancer.Advances in the approach to novel drug clinical development for breast cancer.Embracing synthetic lethality of novel anticancer therapies.Reversing drug resistance of cisplatin by hsp90 inhibitors in human ovarian cancer cells.Biology and Management of Patients With Triple-Negative Breast Cancer.Ganetespib overcomes resistance to PARP inhibitors in breast cancer by targeting core proteins in the DNA repair machinery.Hsp90 induces increased genomic instability toward DNA-damaging agents by tuning down RAD53 transcription.VCP inhibitors induce endoplasmic reticulum stress, cause cell cycle arrest, trigger caspase-mediated cell death and synergistically kill ovarian cancer cells in combination with Salubrinal.Characterization of LGALS3 (galectin-3) as a player in DNA damage response.Cytochrome P450 2A13 is an efficient enzyme in metabolic activation of aflatoxin G1 in human bronchial epithelial cells.Causes and consequences of protein folding stress in aneuploid cells.Boosting the effects of hyperthermia-based anticancer treatments by HSP90 inhibition.Cdc7-Dbf4-mediated phosphorylation of HSP90-S164 stabilizes HSP90-HCLK2-MRN complex to enhance ATR/ATM signaling that overcomes replication stress in cancer.Heat shock proteins and DNA repair mechanisms: an updated overview.Efficacy of Onalespib, a Long-Acting Second-Generation HSP90 Inhibitor, as a Single Agent and in Combination with Temozolomide against Malignant Gliomas.The putative oncogene CEP72 inhibits the mitotic function of BRCA1 and induces chromosomal instability.Somatic mutation of the cohesin complex subunit confers therapeutic vulnerabilities in cancer.Activity of HSP90 Inhibiton in a Metastatic Lung Cancer Patient With a Germline BRCA1 Mutation.Strong antitumor synergy between DNA crosslinking and HSP90 inhibition causes massive premitotic DNA fragmentation in ovarian cancer cells.Proteomic and Bioinformatic Studies for the Characterization of Response to Pemetrexed in Platinum Drug Resistant Ovarian Cancer.
P2860
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P2860
BRCA1 and HSP90 cooperate in homologous and non-homologous DNA double-strand-break repair and G2/M checkpoint activation.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
BRCA1 and HSP90 cooperate in h ...... nd G2/M checkpoint activation.
@ast
BRCA1 and HSP90 cooperate in h ...... nd G2/M checkpoint activation.
@en
type
label
BRCA1 and HSP90 cooperate in h ...... nd G2/M checkpoint activation.
@ast
BRCA1 and HSP90 cooperate in h ...... nd G2/M checkpoint activation.
@en
prefLabel
BRCA1 and HSP90 cooperate in h ...... nd G2/M checkpoint activation.
@ast
BRCA1 and HSP90 cooperate in h ...... nd G2/M checkpoint activation.
@en
P2093
P2860
P356
P1476
BRCA1 and HSP90 cooperate in h ...... nd G2/M checkpoint activation.
@en
P2093
Easwari Kumaraswamy
Fariba Behbod
Lisa M Harlan-Williams
Roy A Jensen
Shane R Stecklein
Vamsee Chaguturu
Wenjia Wang
P2860
P304
13650-13655
P356
10.1073/PNAS.1203326109
P407
P577
2012-08-06T00:00:00Z