CRL4DCAF12regulation of MCMBP ensures optimal licensing of DNA replication DOI Creative Commons
Anoop Yadav, Alikhan Abdirov,

Katarína Ondrušková

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Ноя. 28, 2024

The minichromosome maintenance (MCM2-7) protein complexes are central drivers of genome duplication. Distinct pools, parental and nascent MCMs, their precise equilibrium essential to sustain error-free DNA replication. However, the mechanism responsible for generating these pools maintaining remains largely unexplored. Here, we identified CRL4 DCAF12 as a new factor controlling assembly MCM complexes. During biogenesis, MCMBP facilitates transport newly synthesized MCM3-7 subcomplexes into nucleus. Once in nucleus, MCM2 subunit must be incorporated subcomplex, while needs removed. degradation thereby regulates MCM2-7 absence adversely affects level chromatin-bound resulting accelerated replication forks instability. Collectively, our findings uncovered molecular underlying production counteract instability tumor formation.

Язык: Английский

Single-point mutations in disordered proteins: Linking sequence, ensemble, and function DOI Creative Commons
Eduardo Flores, Nirbhik Acharya, Carlos A. Castañeda

и другие.

Current Opinion in Structural Biology, Год журнала: 2025, Номер 91, С. 102987 - 102987

Опубликована: Фев. 5, 2025

Mutations in genomic DNA often result single-point missense mutations proteins. For folded proteins, the functional effect of these can be understood by their impact on structure. However, intrinsically disordered protein regions (IDRs) remain poorly understood. In IDRs, function depend structural ensemble- collection accessible, interchanging conformations that is encoded amino acid sequence. We argue that, analogously to IDRs alter ensemble, and consequently biological function. To make this argument, we first provide experimental evidence from literature showcasing how affect ensemble dimensions. Then, use data patients show disease-linked occurring can, many cases, significantly IDR ensembles. hope analysis prompts further study disease-linked, IDRs.

Язык: Английский

Процитировано

0

Mechanotransduction in Development: A Focus on Angiogenesis DOI Creative Commons
Simona Alibrandi, Carmela Rinaldi, Sergio Lucio Vinci

и другие.

Biology, Год журнала: 2025, Номер 14(4), С. 346 - 346

Опубликована: Март 27, 2025

Cells respond to external mechanical cues and transduce these forces into biological signals. This process is known as mechanotransduction requires a group of proteins called mechanosensors. peculiar class receptors include extracellular matrix proteins, plasma membrane the cytoskeleton nuclear envelope. These cell components are responsive wide spectrum physical including stiffness, tensile force, hydrostatic pressure shear stress. Among mechanotransducers, Transient Receptor Potential (TRP) PIEZO family members mechanosensitive ion channels, coupling force transduction with intracellular cation transport. Their activity contributes embryo development, tissue remodeling repair, homeostasis. In particular, vessel development driven by hemodynamic such flow direction Perturbed involved in several pathological vascular phenotypes hereditary hemorrhagic telangiectasia. review conceived summarize most recent findings development. We first collected main features proteins. However, we focused on role during Mechanosensitive channels their function also discussed, focus brain morphogenesis.

Язык: Английский

Процитировано

0

Protein folding and quality control during nuclear transport DOI

Sunanda Mallik,

Dylan Poch, Sophia Burick

и другие.

Current Opinion in Cell Biology, Год журнала: 2024, Номер 90, С. 102407 - 102407

Опубликована: Авг. 13, 2024

Язык: Английский

Процитировано

2

CRL4DCAF12regulation of MCMBP ensures optimal licensing of DNA replication DOI Creative Commons
Anoop Yadav, Alikhan Abdirov,

Katarína Ondrušková

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Ноя. 28, 2024

The minichromosome maintenance (MCM2-7) protein complexes are central drivers of genome duplication. Distinct pools, parental and nascent MCMs, their precise equilibrium essential to sustain error-free DNA replication. However, the mechanism responsible for generating these pools maintaining remains largely unexplored. Here, we identified CRL4 DCAF12 as a new factor controlling assembly MCM complexes. During biogenesis, MCMBP facilitates transport newly synthesized MCM3-7 subcomplexes into nucleus. Once in nucleus, MCM2 subunit must be incorporated subcomplex, while needs removed. degradation thereby regulates MCM2-7 absence adversely affects level chromatin-bound resulting accelerated replication forks instability. Collectively, our findings uncovered molecular underlying production counteract instability tumor formation.

Язык: Английский

Процитировано

0