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pro vyhledávání: '"Arvind, Panday"'
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Publikováno v:
STAR Protocols, Vol 3, Iss 3, Pp 101551- (2022)
Summary: In this protocol, we use CRISPR/Cas9 to generate large deletions of the entire coding region of a gene of interest, generating a hemizygous cell line. Next, we systematically engineer precise in-frame deletions within the intact wild-type al
Externí odkaz:
https://doaj.org/article/cf04c21040b54664ad092286e10ec344
Publikováno v:
STAR Protocols, Vol 3, Iss 3, Pp 101529- (2022)
Summary: Chromatin immunoprecipitation coupled with quantitative PCR (ChIP-qPCR) even with optimization may give low signal-to-background ratio and spatial resolution. Here, we adapted Cleavage Under Targets and Release Using Nuclease (CUT&RUN) (orig
Externí odkaz:
https://doaj.org/article/43fea6294a2d47e9bfb4d57950c783a8
Autor:
Rajula Elango, Arvind Panday, Francis P. Lach, Nicholas A. Willis, Kaitlin Nicholson, Erin E. Duffey, Agata Smogorzewska, Ralph Scully
Publikováno v:
Nat Struct Mol Biol
Vertebrate replication forks arrested at interstrand DNA cross-links (ICLs) engage the Fanconi anemia pathway to incise arrested forks, 'unhooking' the ICL and forming a double strand break (DSB) that is repaired by homologous recombination (HR). The
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b21c2311ab2f1f53752438a58784c07a
https://doi.org/10.1038/s41594-022-00812-9
https://doi.org/10.1038/s41594-022-00812-9
Publikováno v:
PLoS Genetics, Vol 14, Iss 7, p e1007486 (2018)
Classical non-homologous end joining (C-NHEJ) and homologous recombination (HR) compete to repair mammalian chromosomal double strand breaks (DSBs). However, C-NHEJ has no impact on HR induced by DNA nicking enzymes. In this case, the replication for
Externí odkaz:
https://doaj.org/article/7e4e077d23e2453286634fff59ee8868
Autor:
Ruoxi W. Wang, Duanduan Ma, Brian Do, Arvind Panday, Sofia Hu, Kate Lu, Matthew G. Vander Heiden, Ralph Scully, Jacqueline A. Lees, Angelika Amon, Xiaofeng A. Su
Publikováno v:
SSRN Electronic Journal.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::e08222e65589b2f46d4721124349e41f
https://doi.org/10.2139/ssrn.4255225
https://doi.org/10.2139/ssrn.4255225
Autor:
Ralph Scully, Rajula Elango, Arvind Panday, Francis Lach, Nicholas Willis, Erin Duffey, Agata Smogorzewska
Vertebrate replication forks arrested at an interstrand DNA crosslink (ICL) can engage the Fanconi anemia (FA) pathway of ICL repair. The FANCP product, SLX4, binds the FANCQ/XPF/ERCC4-ERCC1 endonuclease, which incises bidirectionally arrested forks
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::35402e5ee5e837b5b3602ea04cae835a
https://doi.org/10.21203/rs.3.rs-904746/v1
https://doi.org/10.21203/rs.3.rs-904746/v1
Publikováno v:
Curr Opin Genet Dev
Replication fork stalling occurs when the replisome encounters a barrier to normal fork progression. Replisome stalling events are common during scheduled DNA synthesis, but vary in their severity. At one extreme, a lesion may induce only temporary p
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1baedd9cc1ba5b4ee106f4eda2adbd71
https://europepmc.org/articles/PMC9006750/
https://europepmc.org/articles/PMC9006750/
Autor:
Nicholas A. Willis, Erin E. Duffey, Francesca Menghi, Arvind Panday, Rajula Elango, Ralph Scully, Edison T. Liu
Publikováno v:
Mol Cell
SummaryConservative repair of stalled replication forks is important for the maintenance of a stable genome. However, the mechanisms that regulate repair pathway “choice” at stalled mammalian forks remain poorly understood. The Fanconi anemia com
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::831081ba5d6dde0e2bd541f41dc7557a
https://doi.org/10.1101/2020.10.29.357996
https://doi.org/10.1101/2020.10.29.357996
Autor:
Virginia Camacho, Richard L. Frock, E. Paul Hasty, Ralph Scully, Arvind Panday, Edison T. Liu, Frederick W. Alt, Nicholas A. Willis, Francesca Menghi, Erin E. Duffey
Publikováno v:
Nature
Small, approximately 10-kilobase microhomology-mediated tandem duplications are abundant in the genomes of BRCA1-linked but not BRCA2-linked breast cancer. Here we define the mechanism underlying this rearrangement signature. We show that, in primary
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::cdd56fd7e241f2160cbc55a988320c3e
http://europepmc.org/articles/PMC5728692
http://europepmc.org/articles/PMC5728692