Results 201 to 210 of about 3,838,500 (295)

RSF1‐Dependent PAR Turnover Promotes 53BP1 Liquid Condensate Formation at DNA Damage Sites

open access: yesAdvanced Science, EarlyView.
At sites of DNA damage, RSF1 recruits PARG to accelerate PAR turnover, triggering a switch from PAR‐driven condensates to 53BP1 condensates. This condensate transition enables p53‐dependent gene transcription and coordinates the DNA damage response.
Yungyeong Heo   +10 more
wiley   +1 more source

Computer-Based Design to Improve Bacillus thuringiensis Chitinase for Industrial Applications. [PDF]

open access: yesChemistryOpen
Sree Agash SG   +5 more
europepmc   +1 more source

Compact 9dBEs Enable Efficient and Precise Genome Editing in Mammalian Cells and In Vivo

open access: yesAdvanced Science, EarlyView.
As a compact type II‐D system, the Cas9d‐based platform holds great potential for in vivo applications. Through rational engineering, its derived base editors (9dBEs) enable efficient disease modeling while facilitating single‐vector AAV delivery for in vivo genome editing. These miniature tools offer a robust strategy for basic research and biomedical
Qingquan Xiao   +12 more
wiley   +1 more source

Streptococcal Mannose Phosphotransferase System Component IID Is a Novel RANK‐Binding Osteoclastogenic Factor

open access: yesAdvanced Science, EarlyView.
Streptococcal mannose phosphotransferase system component IID (Man‐PTSIID) is identified as a novel RANK‐binding osteoclastogenic factor. By directly binding to RANK and activating NF‐κB independently of TLR2, Man‐PTSIID drives osteoclastogenesis and inflammatory bone destruction, uncovering an unexpected microbial mechanism underlying streptococcal ...
Chaeyeon Park   +13 more
wiley   +1 more source

Loss of CYLD on Chromosome 16q Impairs Homologous Recombination and Genomic Stability Through TIRR Degradation

open access: yesAdvanced Science, EarlyView.
Chromosome 16q loss drives genomic instability through disruption of the CYLD–TIRR–53BP1 axis. CYLD preserves homologous recombination by stabilizing TIRR and limiting 53BP1 accumulation at DNA double‐strand breaks. CYLD deficiency redirects repair toward error‐prone non‐homologous end joining, promotes mutational burden and homologous recombination ...
Mingming Lu   +14 more
wiley   +1 more source

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