Results 81 to 90 of about 77,894 (293)

Somatic mutational landscape in von Hippel–Lindau familial hemangioblastoma

Molecular Oncology, EarlyView.
The causes of central nervous system (CNS) hemangioblastoma in Von Hippel–Lindau (vHL) disease are unclear. We used Whole Exome Sequencing (WES) on familial hemangioblastoma to investigate events that underlie tumor development. Our findings suggest that VHL loss creates a permissive environment for tumor formation, while additional alterations ...
Maja Dembic, Anne Nørremølle, Lilian Bomme Ousager, Lars van Brakel Andersen, Marie Louise Mølgaard Binderup, Mads Thomassen   +5 more
wiley   +1 more source

Heterozygous loss‐of‐function alleles associate the conserved 3′‐5′ exoribonuclease EXOSC10 with hypersensitivity to the anticancer drug 5‐fluorouracil

Molecular Oncology, EarlyView.
EXOSC10, an essential nuclear RNA exosome‐associated 3′‐5′ exoribonuclease, is inhibited by the anticancer drug 5‐fluorouracil (5‐FU), and EXOSC10 depletion increases 5‐FU sensitivity. The colon‐cancer variant EXOSC10S402T, located in a proteolysis motif, is stable and nuclear but nonfunctional in vivo.
Radhika Sain, Yann Le Page, Frédéric Percevault, Emmanuelle Becker, Luc Negroni, Almudena Fernandez, Marta Cantero, Diego Muñoz‐Santos, Lluís Montoliu, Cyrille Garnier, Michael Primig   +10 more
wiley   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

Molecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober, Leire Moreno‐Cugnon, Laura Martínez‐Pérez, Amaia Ercilla, Amaia Zabala‐Letona, Adrián Vicente‐Barrueco, Maider Fagoaga‐Eugui, Saioa Garcia‐Longarte, Blanca Calle‐Ciborro, Encarnación Pérez‐Andrés, Onintza Carlevaris, Sara Pozo, Isabel Mendizabal, Ugo Mayor, Arkaitz Carracedo, Violaine Sée, Edurne Berra   +16 more
wiley   +1 more source

Characterization of Amino Acid tRNA Ligases using the Analytical Ultracentrifuge [PDF]

, 2015
. Quaternary structures of amino acid tRNA ligases/synthetases (aaRS) in the native as well as in denatured forms were examined by molecular weight determinations (paper I-IV).
Lundvik, Lars
core  

Ubiquitin Ligases: Structure, Function, and Regulation [PDF]

, 2017
Ubiquitin E3 ligases control every aspect of eukaryotic biology by promoting protein ubiquitination and degradation. At the end of a three-enzyme cascade, ubiquitin ligases mediate the transfer of ubiquitin from an E2 ubiquitin-conjugating enzyme to ...
Ning Zheng, Nitzan Shabek
core   +1 more source

E3 Ubiquitin Ligases and Their Therapeutic Applications in Cancers: Narrative Review

Journal of Pharmacy and Bioallied Sciences
E3 ubiquitin ligases are a class of enzymes, essential for maintaining the equilibrium of cells by binding ubiquitin molecules to substrates to mark them for destruction.
Azfar Jamal
doaj   +1 more source

ligases

, 2014
Citation: 'ligases' in the IUPAC Compendium of Chemical Terminology, 3rd ed.; International Union of Pure and Applied Chemistry; 2006. Online version 3.0.1, 2019. 10.1351/goldbook.L03521 • License: The IUPAC Gold Book is licensed under Creative Commons Attribution-ShareAlike CC BY-SA 4.0 International for individual terms. Requests for commercial usage
openaire   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

Molecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder, Klaas de Lint, Hồ Mỹ Phúc Võ, Mariana M. Góis, Rosalie A. Kampen, Marta San Martin Alonso, Ilse Nootenboom, Veronica Garzero, Tiemen J. Wendel, Rob M. F. Wolthuis, Sylvie M. Noordermeer   +10 more
wiley   +1 more source

MITF maintains genome stability in nonmelanocyte lineages

Molecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir, Adrián López García de Lomana, Thejus B. Venkatesh, Kritika Kirty, Snaevar Sigurdsson, Linda Vidarsdottir, Ramile Dilshat, Erla Sveinbjornsdottir, Snaedis Ragnarsdottir, Daniel H Magnusson, Maria R. Bustos, Eirikur Steingrimsson, Thorkell Gudjonsson, Stefan Sigurdsson   +13 more
wiley   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

Molecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu, Nicolas J. Niklaus, Anna M. Schläfli, Igor Tokarchuk, Magali Humbert, Federico La Manna, Bich Vu, David Maul, Ramin Radpour, Marianna Kruithof‐de Julio, Inti Zlobec, Jörn Dengjel, Bruce E. Torbett, Mario P. Tschan   +13 more
wiley   +1 more source