Results 121 to 130 of about 564,359 (343)

A Monte Carlo study of ligand-dependent integrin signal initiation [PDF]

arXiv, 2010
Integrins are allosteric cell adhesion receptors that control many important processes, including cell migration, proliferation, and apoptosis. Ligand binding activates integrins by stabilizing an integrin conformation with separated cytoplasmic tails, thus enabling the binding of proteins that mediate cytoplasmic signaling.
arxiv  

Thermal proteome profiling and proteome analysis using high‐definition mass spectrometry demonstrate modulation of cholesterol biosynthesis by next‐generation galeterone analog VNPP433‐3β in castration‐resistant prostate cancer

Molecular Oncology, EarlyView.
Elevated level of cholesterol is positively correlated to prostate cancer development and disease severity. Cholesterol‐lowering drugs, such as statins, are demonstrated to inhibit prostate cancer. VNPP433‐3β interrupts multiple signaling and metabolic pathways, including cholesterol biosynthesis, AR‐mediated transcription of several oncogenes, mRNA 5′
Retheesh S. Thankan, Elizabeth Thomas, Mehari M. Weldemariam, Puranik Purushottamachar, Weiliang Huang, Maureen A. Kane, Yuji Zhang, Nicholas Ambulos, Bi‐Dar Wang, David Weber, Vincent C. O. Njar   +10 more
wiley   +1 more source

Affinity labeling of the catalytic subunit of cyclic AMP-dependent protein kinase by N alpha-tosyl-L-lysine chloromethyl ketone. [PDF]

, 1979
Abraham Kupfer, Viviane Gani, Juan S. Jiménez, Shmuel Shaltiel   +3 more
openalex   +1 more source

Elucidating prognostic significance of purine metabolism in colorectal cancer through integrating data from transcriptomic, immunohistochemical, and single‐cell RNA sequencing analysis

Molecular Oncology, EarlyView.
Low expression of five purine metabolism‐related genes (ADSL, APRT, ADCY3, NME3, NME6) was correlated with poor survival in colorectal cancer. Immunohistochemistry analysis showed that low NME3 (early stage) and low ADSL/NME6 (late stage) levels were associated with high risk.
Sungyeon Kim, Myunghee Kang, Soyeon Jeong, Jisup Kim, Kyoung Oh Kim, Won‐Suk Lee, Jeong‐Heum Baek, Jung Ho Kim, Seungyoon Nam   +8 more
wiley   +1 more source

Nuclear protein kinase activity in glucagon-stimulated perfused rat livers [PDF]

, 1974
W. K. Palmer, Monique Castagna, Donal A. Walsh   +2 more
openalex   +1 more source

The atypical KRASQ22K mutation directs TGF‐β response towards partial epithelial‐to‐mesenchymal transition in patient‐derived colorectal cancer tumoroids

Molecular Oncology, EarlyView.
TGF‐β has a complex role in cancer, exhibiting both tumor‐suppressive and tumor‐promoting properties. Using a series of differentiated tumoroids, derived from different stages and mutational background of colorectal cancer patients, we replicate this duality of TGF‐β in vitro. Notably, the atypical but highly aggressive KRASQ22K mutation rendered early‐
Theresia Mair, Philip König, Milena Mijović, Jessica Kalla, Anil Baskan, Loan Tran, Kristina Draganić, Pedro Morata Saldaña, Carlos Uziel Pérez Malla, Janette Pfneissl, Andreas Tiefenbacher, Julijan Kabiljo, Velina S. Atanasova, Lisa Wozelka‐Oltjan, Leonhard Müllauer, Michael Bergmann, Raheleh Sheibani‐Tezerji, Gerda Egger   +17 more
wiley   +1 more source

Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal‐like and malignant urothelial cells

Molecular Oncology, EarlyView.
Loss of the frequently mutated chromatin remodeler ARID1A, a subunit of the SWI/SNF cBAF complex, results in less open chromatin, alternative splicing, and the failure to stop cells from progressing through the cell cycle after DNA damage in bladder (cancer) cells. Created in BioRender. Epigenetic regulators, such as the SWI/SNF complex, with important
Rebecca M. Schlösser, Florian Krumbach, Eyleen Corrales, Geoffroy Andrieux, Christian Preisinger, Franziska Liss, Alexandra Golzmann, Melanie Boerries, Kerstin Becker, Ruth Knüchel, Stefan Garczyk, Bernhard Lüscher   +11 more
wiley   +1 more source

Germline variants in CDKN2A wild‐type melanoma prone families

Molecular Oncology, EarlyView.
Among melanoma‐prone families, wild‐type for CDKN2A and CDK4, some have pathogenic variants in genes not usually linked to melanoma. Furthermore, rare XP‐related variants and variants in MC1R are enriched in such families. Germline pathogenic variants in CDKN2A are well established as an underlying cause of familial malignant melanoma. While pathogenic
Gjertrud T. Iversen, Marie Loeng, Amalie Lund Holth, Per E. Lønning, Jürgen Geisler, Stian Knappskog   +5 more
wiley   +1 more source

Escape from TGF‐β‐induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

Molecular Oncology, EarlyView.
Chronic TGF‐β exposure drives epithelial HCC cells from a senescent state to a TGF‐β resistant mesenchymal phenotype. This transition is characterized by the loss of Smad3‐mediated signaling, escape from senescence, enhanced invasiveness and metastatic potential, and upregulation of key resistance modulators such as MARK1 and GRM8, ultimately promoting
Minenur Kalyoncu, Dilara Demirci, Sude Eris, Bengisu Dayanc, Ece Cakiroglu, Merve Basol, Merve Uysal, Gulcin Cakan‐Akdogan, Fang Liu, Mehmet Ozturk, Gökhan Karakülah, Serif Senturk   +11 more
wiley   +1 more source

ShcD adaptor protein drives invasion of triple negative breast cancer cells by aberrant activation of EGFR signaling

Molecular Oncology, EarlyView.
We identified adaptor protein ShcD as upregulated in triple‐negative breast cancer and found its expression to be correlated with reduced patient survival and increased invasion in cell models. Using a proteomic screen, we identified novel ShcD binding partners involved in EGFR signaling pathways.
Hayley R. Lau, Hayley S. Smith, Begüm Alural, Claire E. Martin, Laura A. New, Manali Tilak, Sara L. Banerjee, Hannah N. Robeson, Nicolas Bisson, Anne‐Claude Gingras, Jasmin Lalonde, Nina Jones   +11 more
wiley   +1 more source