Zobrazeno 1 - 10
of 15
pro vyhledávání: '"Lavinia C. Dumitrache"'
Autor:
Paul Hasty, Thomas Ried, Hesed Padilla-Nash, Sheng-Mei Ma, Danny Wangsa, Lavinia C. Dumitrache, Ming-Jiu Chen
Supplementary Table 1 from Cisplatin Depletes TREX2 and Causes Robertsonian Translocations as Seen in TREX2 Knockout Cells
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::04091477dc55286b2c225351fb7e7c68
https://doi.org/10.1158/0008-5472.22371687
https://doi.org/10.1158/0008-5472.22371687
Autor:
Paul Hasty, Thomas Ried, Hesed Padilla-Nash, Sheng-Mei Ma, Danny Wangsa, Lavinia C. Dumitrache, Ming-Jiu Chen
Cisplatin, an anticancer drug, forms DNA interstrand cross-links (ICL) that interfere with replication, whereas TREX2 is a 3′→5′ exonuclease that removes 3′ mismatched nucleotides and promotes cellular proliferation. Here, we show that TREX2
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::bc91ce8e12cad95f56cfca7aef6d46c7
https://doi.org/10.1158/0008-5472.c.6496887
https://doi.org/10.1158/0008-5472.c.6496887
Publikováno v:
Neuron. 110:3217-3219
Abnormal activity of LINE-1 transposable elements has been associated with neurological disease. In this issue of Neuron, Takahashi et al. (2022) show that L1 hyperactivity occurs in the neurodegenerative syndrome ataxia telangiectasia and causes ata
Autor:
Young Don Kwak, Timothy I. Shaw, Susanna M. Downing, Ambika Tewari, Hongjian Jin, Yang Li, Lavinia C. Dumitrache, Sachin Katyal, Kamran Khodakhah, Helen R. Russell, Peter J. McKinnon
Publikováno v:
Science advances. 7(51)
The pathogenesis of inherited genome instability neurodegenerative syndromes remains largely unknown. Here, we report new disease-relevant murine models of genome instability–driven neurodegeneration involving disabled ATM and APTX that develop deb
Autor:
Momoko Ishikawa, André Nussenzweig, Peter J. McKinnon, Michelle E. Ehrlich, Andre Stanlie, Nancy Wong, Wei Wu, Frida Belinky, Dali Zong, Kenta Shinoda, Lavinia C. Dumitrache, Elsa Callen
The Shieldin complex, consisting of SHLD1, SHLD2, SHLD3 and REV7, shields DNA double strand breaks (DSBs) from nucleolytic resection. The end-protecting activity of Shieldin promotes productive non-homologous end joining (NHEJ) in G1 but can threaten
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::7a392b928dbc5ee9661a5b3c17a52908
https://doi.org/10.1101/2020.07.19.210773
https://doi.org/10.1101/2020.07.19.210773
Publikováno v:
Mechanisms of Ageing and Development. 161:121-129
A variety of human neurologic diseases are caused by inherited defects in DNA repair. In many cases, these syndromes almost exclusively impact the nervous system, underscoring the critical requirement for genome stability in this tissue. A striking e
Autor:
Jennifer L. Illuzzi, Helen R. Russell, Peter J. McKinnon, David M. Wilson, Yang Li, Susanna M. Downing, Mikio Shimada, Young-Don Kwak, Lavinia C. Dumitrache
Frequent oxidative modification of the neural genome is a by-product of the high oxygen consumption of the nervous system. Rapid correction of oxidative DNA lesions is essential, as genome stability is a paramount determinant of neural homeostasis. A
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a9b474dc5b1e438915ad7625d9aa4dea
https://europepmc.org/articles/PMC6310806/
https://europepmc.org/articles/PMC6310806/
Autor:
Jeremy M. Stark, Andrea K. Byrum, Elsa Callen, Nancy Wong, Andre Stanlie, Yaakov Maman, Nima Mosammaparast, Raphael Souza Pavani, Michael J. Kruhlak, Amanda Day, Wei Wu, André Nussenzweig, Lavinia C. Dumitrache, Peter J. McKinnon, Dali Zong, Andres Canela, Maria A. Blasco, Carlos Mendez-Dorantes, Paula Martinez, Momoko Ishikawa
Publikováno v:
Mol Cell
Summary 53BP1 activity drives genome instability and lethality in BRCA1-deficient mice by inhibiting homologous recombination (HR). The anti-recombinogenic functions of 53BP1 require phosphorylation-dependent interactions with PTIP and RIF1/shieldin
Publikováno v:
The EMBO Journal. 34:2465-2480
Polynucleotide kinase–phosphatase (PNKP) is a DNA repair factor possessing both 5′‐kinase and 3′‐phosphatase activities to modify ends of a DNA break prior to ligation. Recently, decreased PNKP levels were identified as the cause of severe
Autor:
Eric J. Brown, Vanessa Enriquez-Rios, Helen R. Russell, Susanna M. Downing, Peter J. McKinnon, Lavinia C. Dumitrache, Yang Li
The DNA damage response (DDR) orchestrates a network of cellular processes that integrates cell-cycle control and DNA repair or apoptosis, which serves to maintain genome stability. DNA-PKcs (the catalytic subunit of the DNA-dependent kinase, encoded
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::73544dde4fca7872785d960692191907
https://europepmc.org/articles/PMC5296783/
https://europepmc.org/articles/PMC5296783/