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Salgia, Ravi
One or more keywords matched the following items that are connected to Salgia, Ravi
Item TypeName
Concept Transfection
Academic Article p210BCR/ABL induces formation of complexes containing focal adhesion proteins and the protooncogene product p120c-Cbl.
Academic Article Interleukin-3 and p210 BCR/ABL activate both unique and overlapping pathways of signal transduction in a factor-dependent myeloid cell line.
Academic Article BCR/ABL induces multiple abnormalities of cytoskeletal function.
Academic Article The noncatalytic domain of protein-tyrosine phosphatase-PEST targets paxillin for dephosphorylation in vivo.
Academic Article Differential expression and signaling of CBL and CBL-B in BCR/ABL transformed cells.
Academic Article BAL is a novel risk-related gene in diffuse large B-cell lymphomas that enhances cellular migration.
Academic Article c-MET mutational analysis in small cell lung cancer: novel juxtamembrane domain mutations regulating cytoskeletal functions.
Academic Article Expression of Siva-1 protein or its putative amphipathic helical region enhances cisplatin-induced apoptosis in breast cancer cells: effect of elevated levels of BCL-2.
Academic Article The MET receptor tyrosine kinase is a potential novel therapeutic target for head and neck squamous cell carcinoma.
Academic Article EphA2 mutation in lung squamous cell carcinoma promotes increased cell survival, cell invasion, focal adhesions, and mammalian target of rapamycin activation.
Academic Article c-Met is a potentially new therapeutic target for treatment of human melanoma.
Academic Article Shc phosphorylation in myeloid cells is regulated by granulocyte macrophage colony-stimulating factor, interleukin-3, and steel factor and is constitutively increased by p210BCR/ABL.
Academic Article The thrombopoietin receptor c-MPL activates JAK2 and TYK2 tyrosine kinases.
Academic Article An E3 ubiquitin ligase: c-Cbl: a new therapeutic target of lung cancer.
Academic Article AXL mediates resistance to cetuximab therapy.
Academic Article Met gene amplification and protein hyperactivation is a mechanism of resistance to both first and third generation EGFR inhibitors in lung cancer treatment.
Academic Article USP22 Interacts with PALB2 and Promotes Chemotherapy Resistance via Homologous Recombination of DNA Double-Strand Breaks.
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  • Transfection