CCDC98 is a BRCA1-BRCT domain–binding protein involved in the DNA damage response

2007 ◽  
Vol 14 (8) ◽  
pp. 710-715 ◽  
Author(s):  
Hongtae Kim ◽  
Jun Huang ◽  
Junjie Chen
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Binding Protein ◽  
Brct Domain ◽  
Damage Response

scholarly journals INTS3 controls the hSSB1-mediated DNA damage response

2009 ◽  
Vol 187 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Jeffrey R. Skaar ◽  
Derek J. Richard ◽  
Anita Saraf ◽  
Alfredo Toschi ◽  
Emma Bolderson ◽  
...  
Keyword(s):  
Dna Damage ◽  
Signaling Pathway ◽  
Dna Damage Response ◽  
Ataxia Telangiectasia ◽  
Binding Protein ◽  
Ataxia Telangiectasia Mutated ◽  
Uncharacterized Protein ◽  
Damage Response ◽  
Atm Signaling Pathway ◽  
Atm Signaling

Human SSB1 (single-stranded binding protein 1 [hSSB1]) was recently identified as a part of the ataxia telangiectasia mutated (ATM) signaling pathway. To investigate hSSB1 function, we performed tandem affinity purifications of hSSB1 mutants mimicking the unphosphorylated and ATM-phosphorylated states. Both hSSB1 mutants copurified a subset of Integrator complex subunits and the uncharacterized protein LOC58493/c9orf80 (henceforth minute INTS3/hSSB-associated element [MISE]). The INTS3–MISE–hSSB1 complex plays a key role in ATM activation and RAD51 recruitment to DNA damage foci during the response to genotoxic stresses. These effects on the DNA damage response are caused by the control of hSSB1 transcription via INTS3, demonstrating a new network controlling hSSB1 function.

scholarly journals Suppressor mutations in Mecp2-null mice reveal that the DNA damage response is key to Rett syndrome pathology

2019 ◽  
Author(s):  
Adebola Enikanolaiye ◽  
Julie Ruston ◽  
Rong Zeng ◽  
Christine Taylor ◽  
Marijke Shrock ◽  
...  
Keyword(s):  
Dna Damage ◽  
Candidate Genes ◽  
Rett Syndrome ◽  
Association Analysis ◽  
Dna Damage Response ◽  
Binding Protein ◽  
Symptom Improvement ◽  
Suppressor Mutations ◽  
Entry Points ◽  
Damage Response

AbstractMutations in X-linked methyl-CpG-binding protein 2 (MECP2) cause Rett syndrome (RTT). We carried out a genetic screen for secondary mutations that improved phenotypes in Mecp2/Y mice after mutagenesis with N-ethyl-N-nitrosourea (ENU), aiming to identify potential therapeutic entry points. Here we report the isolation of 106 founder animals that show suppression of Mecp2-null traits from screening 3,177 Mecp2/Y genomes. Using exome sequencing, genetic crosses and association analysis, we identify 33 candidate genes in 30 of the suppressor lines. A network analysis shows that 61% of the candidate genes cluster into the functional categories of transcriptional repression, chromatin modification or DNA repair, delineating a pathway relationship with MECP2. Many mutations lie in genes that are predicted to modulate synaptic signaling or lipid homeostasis. Surprisingly, mutations in genes that function in the DNA damage response (DDR) also improve symptoms in Mecp2/Y mice. The combinatorial effects of multiple loci can be resolved by employing association analysis. One line, which was previously reported to carry a suppressor mutation in a gene required for cholesterol synthesis, Sqle, carries a second mutation in retinoblastoma binding protein 8 (Rbbp8 or CtIP), which regulates a DDR choice in double stranded break (DSB) repair. Cells from Mecp2/Y mice have increased DSBs, so this finding suggests that the balance between homology directed repair and non-homologous end joining is important for neuronal cells. In this and other lines, the presence of two suppressor mutations confers better symptom improvement than one locus alone, suggesting that combination therapies could be effective in RTT.

scholarly journals Immunofluorescence analysis of DNA damage response protein p53-binding protein 1 in a case of uterine dedifferentiated leiomyosarcoma arising from leiomyoma

2019 ◽  
Vol 215 (11) ◽  
pp. 152640
Author(s):  
Katsuya Matsuda ◽  
Yuko Akazawa ◽  
Yuka Yamaguchi ◽  
Zhanna Mussazhanova ◽  
Hirokazu Kurohama ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Binding Protein ◽  
Immunofluorescence Analysis ◽  
Protein P53 ◽  
Damage Response

Abstract A18: HuR, an RNA binding protein, is critical for the DNA damage response in pancreatic cancer cells.

2012 ◽  
Author(s):  
Shruti Lal ◽  
Vikram Bhattacharjee ◽  
Timothy Yen ◽  
Richard A. Burkhart ◽  
Danielle M. Pineda ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Pancreatic Cancer Cells ◽  
Damage Response

scholarly journals PARP activation regulates the RNA-binding protein NONO in the DNA damage response to DNA double-strand breaks

2012 ◽  
Vol 40 (20) ◽  
pp. 10287-10301 ◽  
Author(s):  
Jana Krietsch ◽  
Marie-Christine Caron ◽  
Jean-Philippe Gagné ◽  
Chantal Ethier ◽  
Julien Vignard ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Parp Activation ◽  
Strand Breaks ◽  
Damage Response
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