Results 71 to 80 of about 182,107 (250)

Predicted missing information biases ensemble perception of temporally ordered facial expressions

Scientific Reports
By observing dynamically changing facial expressions, humans can use a specialized capacity known as ensemble coding to effortlessly obtain a summary representation of an individual’s emotional state.
Jiahao Lu, Jun Wang
doaj   +1 more source

The Shewanella oneidensis Fic enzyme SoFic targets the switch‐I region of EF‐Tu for AMPylation

FEBS Letters, EarlyView.
Fic enzymes mediate diverse post‐translational modifications across all domains of life, including AMPylation. Prokaryotic EF‐Tu can be AMPylated and deAMPylated by the conserved Fic enzyme SoFic. Structural and biochemical approaches were used to characterize the effect of AMPylation on EF‐Tu, SoFic's enzymatic activities, and the enzyme‐target ...
Svenja Runge, Vivian Pogenberg, Alexander Baumgart, Bente Siebels, Hartmut Schlüter, Michael Hecht‐Bucher, Aymelt Itzen   +6 more
wiley   +1 more source

The heterodimeric amino acid transporters (HAT) of the SLC7/SLC3 family: A structure−function relationships and relevance to human pathology

FEBS Letters, EarlyView.
Heterodimeric amino acid transporters consist of SLC7 and SLC3 family proteins arranged in a conserved structural organization. They regulate nutrient transport across cell membranes, supporting essential cellular functions. These transporters also contribute to xenobiotic/drug uptake and distribution.
Mariafrancesca Scalise, Tiziano Mazza, Raffaella Scanga, Lara Console, Michele Galluccio, Cesare Indiveri   +5 more
wiley   +1 more source

The role of miR‐335‐5p in the redifferentiation of BRAF p.V600E thyroid cancers

Molecular Oncology, EarlyView.
The BRAF p.V600E mutation promotes thyroid cancer dedifferentiation and radioiodine resistance. Using a network approach, we identified miR‐335‐5p as a key regulator of BRAF‐mutated thyroid tumors. Restoring miR‐335‐5p increased thyroid‐specific gene expression and iodine uptake in cells and organoids.
Valeria Pecce, Simone Bini, Marialuisa Sponziello, Giorgio Grani, Giulia Fiscon, Paola Paci, Lorenzo Farina, Rosa Falcone, Valentina Maggisano, Sebastiano Filetti, Cosimo Durante, Antonella Verrienti   +11 more
wiley   +1 more source

Circular RNA expression landscapes in myelodysplastic neoplasms: Associations with mutational signatures and disease progression

Molecular Oncology, EarlyView.
In this explorative study, the abundance of circular RNA molecules in bone marrow stem cells was found to be elevated in patients with high‐risk myelodysplastic neoplasms, and to be associated with an increased risk of progression to acute myeloid leukemia.
Eileen Wedge, Morten Tulstrup, Gabriele Todisco, Pedro Moura, Christophe Côme, Jakob Werner Hansen, Jakob Schmidt Jespersen, Balthasar Schlotmann, Maria Creignou, Mette Dahl, Claudia Schöllkopf, Klas Raaschou‐Jensen, Krister Wennerberg, Bo Porse, Joachim Weischenfeldt, Eva Hellström‐Lindberg, Lasse Sommer Kristensen, Kirsten Grønbæk   +17 more
wiley   +1 more source

Transcriptional profiling of circulating extracellular vesicles from prebiopsy prostate cancer patients

Molecular Oncology, EarlyView.
RNA profiling of circulating extracellular vesicles (EVs) from blood samples of men undergoing prostate biopsy identifies transcripts associated with clinically significant prostate cancer. Integrative analysis with public tumor datasets links EV‐derived gene signatures to tumor stage and progression‐free survival, highlighting CASP3, XRCC2, and RIT1 ...
Stefan Werner, Pierre Tennstedt, Randi C. Pose, Christian Müller, Katharina Besler, Svenja Schneegans, Malik Alawi, Marie C. Roesch, Sven Peine, Desiree Bonci, Joanna Budna‐Tukan, Evi Lianidou, Catherine Alix‐Panabières, Derya Tilki, Klaus Pantel   +14 more
wiley   +1 more source

Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma

Molecular Oncology, EarlyView.
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska, Stephany Gallardo, Nur S. Zainal, Leena Arora, Matthew Ellis, Maria‐Antoinette Lopez, Judith Austine, Sai Pittla, Serena J Chee, Aiman Alzetani, Emily C Shaw, Christian H Ottensmeier, Gareth J Thomas, Christopher J Hanley   +13 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

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