Results 121 to 130 of about 1,043,830 (367)

MET variants with activating N‐lobe mutations identified in hereditary papillary renal cell carcinomas still require ligand stimulation

Molecular Oncology, EarlyView.
MET variants in the N‐lobe of the kinase domain, found in hereditary papillary renal cell carcinoma, require ligand stimulation to promote cell transformation, in contrast to other RTK variants. This suggests that HGF expression in the microenvironment is important for tumor growth in such patients. Their sensitivity to MET inhibitors opens the way for
Célia Guérin, Audrey Vinchent, Marie Fernandes, Isabelle Damour, Agathe Laratte, Rémi Tellier, Gabriella O. Estevam, Jean‐Pascal Meneboo, Céline Villenet, Clotilde Descarpentries, James S. Fraser, Martin Figeac, Alexis B. Cortot, Etienne Rouleau, David Tulasne   +14 more
wiley   +1 more source

Fcgamma receptor-mediated phagocytosis in macrophages lacking the Src family tyrosine kinases Hck, Fgr, and Lyn. [PDF]

, 2000
Macrophage Fcgamma receptors (FcgammaRs) mediate the uptake and destruction of antibody-coated viruses, bacteria, and parasites. We examined FcgammaR signaling and phagocytic function in bone marrow-derived macrophages from mutant mice lacking the major ...
Crowley, MT, DeFranco, AL, Finn, AJ, Fitzer-Attas, CJ, Lowell, CA, Lowry, M, Meng, F   +6 more
core  

MAP kinase pathway alterations in BRAF-mutant melanoma patients with acquired resistance to combined RAF/MEK inhibition.

Cancer Discovery, 2014
Treatment of BRAF-mutant melanoma with combined dabrafenib and trametinib, which target RAF and the downstream MAP-ERK kinase (MEK)1 and MEK2 kinases, respectively, improves progression-free survival and response rates compared with dabrafenib ...
N. Wagle, E. V. Van Allen, D. Treacy, Dennie T. Frederick, Z. Cooper, A. Taylor-Weiner, Mara W Rosenberg, Eva M. Goetz, R. Sullivan, Deborah N. Farlow, Dennis C. Friedrich, K. Anderka, Danielle L Perrin, Cory M. Johannessen, A. McKenna, K. Cibulskis, G. Kryukov, Eran Hodis, D. Lawrence, Sheila A Fisher, G. Getz, S. Gabriel, S. Carter, K. Flaherty, J. Wargo, L. Garraway   +25 more
semanticscholar   +1 more source

Etoposide‐induced cancer cell death: roles of mitochondrial VDAC1 and calpain, and resistance mechanisms

Molecular Oncology, EarlyView.
The complex mode of action of the topoisomerase II inhibitor etoposide in triggering apoptosis involves several mechanisms: overexpression of the mitochondrial protein VDAC1, leading to its oligomerization and formation of a large channel that mediates the release of pro‐apoptotic protein; and overexpression of the apoptosis regulators p53, Bax, and ...
Aditya Karunanithi Nivedita, Varda Shoshan‐Barmatz   +1 more
wiley   +1 more source

3D-QSAR models to predict anti-cancer activity on a series of protein P38 MAP kinase inhibitors

Journal of Taibah University for Science, 2017
Protein kinases are essential components of various signaling pathways and represent attractive targets for therapeutic interventions. Kinase inhibitors are currently used to treat malignant tumors, as well as autoimmune diseases, due to their ...
El Ghalia Hadaji, Mohamed Bourass, Abdelkarim Ouammou, Mohammed Bouachrine   +3 more
doaj   +1 more source

Integrins can collaborate with growth factors for phosphorylation of receptor tyrosine kinases and MAP kinase activation: roles of integrin aggregation and occupancy of receptors

Journal of Cell Biology, 1996
Integrins mediate cell adhesion, migration, and a variety of signal transduction events. These integrin actions can overlap or even synergize with those of growth factors.
S. Miyamoto, H. Teramoto, J. Gutkind, K. Yamada   +3 more
semanticscholar   +1 more source

Respiratory complex I‐mediated NAD+ regeneration regulates cancer cell proliferation through the transcriptional and translational control of p21Cip1 expression by SIRT3 and SIRT7

Molecular Oncology, EarlyView.
NAD+ regeneration by mitochondrial complex I NADH dehydrogenase is important for cancer cell proliferation. Specifically, NAD+ is necessary for the activities of NAD+‐dependent deacetylases SIRT3 and SIRT7, which suppress the expression of p21Cip1 cyclin‐dependent kinase inhibitor, an antiproliferative molecule, at the translational and transcriptional
Masato Higurashi, Kazunori Mori, Hidetsugu Nakagawa, Momoko Uchida, Fumihiro Ishikawa, Motoko Shibanuma   +5 more
wiley   +1 more source

Molecular and functional profiling unravels targetable vulnerabilities in colorectal cancer

Molecular Oncology, EarlyView.
We used whole exome and RNA‐sequencing to profile divergent genomic and transcriptomic landscapes of microsatellite stable (MSS) and microsatellite instable (MSI) colorectal cancer. Alterations were classified using a computational score for integrative cancer variant annotation and prioritization.
Efstathios‐Iason Vlachavas, Konstantinos Voutetakis, Vivian Kosmidou, Spyridon Tsikalakis, Spyridon Roditis, Konstantinos Pateas, Ryangguk Kim, Kymberleigh Pagel, Stephan Wolf, Gregor Warsow, Antonia Dimitrakopoulou‐Strauss, Georgios N. Zografos, Alexander Pintzas, Johannes Betge, Olga Papadodima, Stefan Wiemann   +15 more
wiley   +1 more source

Stochastic variation in the FOXM1 transcription program mediates replication stress tolerance

Molecular Oncology, EarlyView.
Cellular heterogeneity is a major cause of drug resistance in cancer. Segeren et al. used single‐cell transcriptomics to investigate gene expression events that correlate with sensitivity to the DNA‐damaging drugs gemcitabine and prexasertib. They show that dampened expression of transcription factor FOXM1 and its target genes protected cells against ...
Hendrika A. Segeren, Kathryn A. Wierenga, Frank M. Riemers, Elsbeth A. van Liere, Bart Westendorp   +4 more
wiley   +1 more source

Selective Activation of p38 Mitogen-activated Protein (MAP) Kinase Isoforms by the MAP Kinase Kinases MKK3 and MKK6*

Journal of Biological Chemistry, 1998
The cellular response to treatment with proinflammatory cytokines or exposure to environmental stress is mediated, in part, by the p38 group of mitogen-activated protein (MAP) kinases. We report the molecular cloning of a novel isoform of p38 MAP kinase,
H. Enslen, J. Raingeaud, R. Davis
semanticscholar   +1 more source