Results 111 to 120 of about 3,572,003 (397)
β‐TrCP overexpression enhances cisplatin sensitivity by depleting BRCA1
Molecular Oncology, EarlyView.Low levels of β‐TrCP (Panel A) allow the accumulation of BRCA1 and CtIP, which facilitate the repair of cisplatin‐induced DNA damage via homologous recombination (HR) and promote tumor cell survival. In contrast, high β‐TrCP expression (Panel B) leads to BRCA1 and CtIP degradation, impairing HR repair, resulting in persistent DNA damage and apoptosis ...
Rocío Jiménez‐Guerrero +8 more
wiley +1 more source
ORM Promotes Skeletal Muscle Glycogen Accumulation via CCR5-Activated AMPK Pathway in Mice
Frontiers in Pharmacology, 2016 We found previously that acute phase protein orosomucoid reacts to fatigue and activates C-C chemokine receptor type 5 to increase muscle glycogen storage and enhance muscle endurance (Lei et al., 2016). To explore the underlying molecular mechanisms, we
Zhen Qin +6 more
doaj +1 more source
Identification of a Phosphorylation Site for Calcium/Calmodulindependent Protein Kinase II in the NR2B Subunit of the N-Methyl-D-aspartate Receptor [PDF]
, 1996 The N-methyl-D-aspartate (NMDA) subtype of excitatory glutamate receptors plays critical roles in embryonic and adult synaptic plasticity in the central nervous system.
Alan J. Rosenstein +51 more
core +1 more source
Molecular Oncology, EarlyView.AZD9291 has shown promise in targeted cancer therapy but is limited by resistance. In this study, we employed metabolic labeling and LC–MS/MS to profile time‐resolved nascent protein perturbations, allowing dynamic tracking of drug‐responsive proteins. We demonstrated that increased NNMT expression is associated with drug resistance, highlighting NNMT ...
Zhanwu Hou +5 more
wiley +1 more source
Molecular Oncology, EarlyView.A‐to‐I editing of miRNAs, particularly miR‐200b‐3p, contributes to HGSOC progression by enhancing cancer cell proliferation, migration and 3D growth. The edited form is linked to poorer patient survival and the identification of novel molecular targets.
Magdalena Niemira +14 more
wiley +1 more source
Molecular Oncology, EarlyView.This study indicates that Merkel cell carcinoma (MCC) does not originate from Merkel cells, and identifies gene, protein & cellular expression of immune‐linked and neuroendocrine markers in primary and metastatic Merkel cell carcinoma (MCC) tumor samples, linked to Merkel cell polyomavirus (MCPyV) status, with enrichment of B‐cell and other immune cell
Richie Jeremian +10 more
wiley +1 more source
Tumor Biology, 2017 We previously reported that 37-kDa laminin receptor precursor involved in metastasis of lung adenocarcinoma cancer cells. In this study, we further revealed that hypoxia induced 37-kDa laminin receptor precursor expression and activation of extracellular
Yongan Zhou +6 more
doaj +1 more source
Activation of type II calcium/calmodulin-dependent protein kinase by Ca^(2+)/calmodulin is inhibited by autophosphorylation of threonine within the calmodulin-binding domain [PDF]
, 1990 It is now well established that autophosphorylation of a threonine residue located next to each calmodulin-binding domain in the subunits of type II Ca^(2+)/calmodulin-dependent protein kinase causes the kinase to remain active, although at a reduced ...
Kennedy, Mary B. +2 more
core
YAP1::TFE3 mediates endothelial‐to‐mesenchymal plasticity in epithelioid hemangioendothelioma
Molecular Oncology, EarlyView.The YAP1::TFE3 fusion protein drives endothelial‐to‐mesenchymal transition (EndMT) plasticity, resulting in the loss of endothelial characteristics and gain of mesenchymal‐like properties, including resistance to anoikis, increased migratory capacity, and loss of contact growth inhibition in endothelial cells.
Ant Murphy +9 more
wiley +1 more source
International Journal of Biological Sciences, 2006 Protein dephosphorylation by protein phosphatase 1 (PP1), acting in concert with protein kinase C (PKC) and protein kinase A (PKA), is a pivotal regulatory mechanism of protein phosphorylation.
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