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Detection and Quantitation of Endogenous Membrane-Bound RAS Proteins and KRAS Mutants in Cancer Cell Lines Using 1D-SDS-PAGE LC-MS.
Methods Mol Biol
July 2024
Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.
In healthy cells, membrane-anchored wild-type RAS proteins (i.e., HRAS, KRAS4A, KRAS4B, and NRAS) regulate critical cellular processes (e.
View Article and Find Full Text PDFPatterning of Oncogenic Ras Clustering in Live Cells Using Vertically Aligned Nanostructure Arrays.
Nano Lett
February 2022
School of Chemical and Biomedical Engineering, Nanyang Technological University, Singapore 637457, Singapore.
As a dominant oncogenic protein, Ras is well-known to segregate into clusters on the plasma membrane for activating downstream signaling. However, current technologies for direct measurements of Ras clustering are limited to sophisticated high-resolution techniques like electron microscopy and fluorescence lifetime imaging. To further promote fundamental investigations and the related drug development, we hereby introduce a nanobar-based platform which effectively guides Ras clusters into quantifiable patterns in live cells that is resolvable under conventional microscopy.
View Article and Find Full Text PDFRAS specific protease induces irreversible growth arrest via p27 in several KRAS mutant colorectal cancer cell lines.
Sci Rep
September 2021
Department of Microbiology and Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Ras-specific proteases to degrade RAS within cancer cells are under active development as an innovative strategy to treat tumorigenesis. The naturally occurring biological toxin effector called RAS/RAP1-specific endopeptidase (RRSP) is known to cleave all RAS within a cell, including HRAS, KRAS, NRAS and mutant KRAS G13D. Yet, our understanding of the mechanisms by which RRSP drives growth inhibition are unknown.
View Article and Find Full Text PDFKRAS mutations in patients with colorectal cancer in Libya.
Mol Clin Oncol
October 2021
Biotechnology Research Centre, National Cancer Institute-Misurata, Misurata 218-51, Libya.
Large prospective clinical trials have demonstrated that colorectal cancers (CRCs) with wild-type KRAS respond favorably to anti-epidermal growth factor receptor treatment, thus making mutational analysis obligatory prior to treatment. In our study, frozen CRC tissues from Libyan patients were analyzed for KRAS and HRAS mutations in codons 12/13 by direct sequencing and the correlations with clinical and pathological parameters were investigated. A total of 34 CRC cases, comprising 19 men and 15 women (age range, 24-87 years), were subjected to systematic analysis for RAS mutations.
View Article and Find Full Text PDFDiscernment between candidate mechanisms for KRAS G13D colorectal cancer sensitivity to EGFR inhibitors.
Cell Commun Signal
November 2020
Integrative Biology Laboratory, Salk Institute for Biological Studies, 10010 N. Torrey Pines Rd, La Jolla, CA, 92037, USA.
Phase three clinical trial evidence suggests that colorectal cancers with the KRAS G13D mutation may benefit from EGFR inhibitors, like cetuximab, in contrast to the other most common KRAS mutations. A mechanism to explain why this mutation behaves differently from other KRAS mutations had long been lacking. Two recent studies have reproduced KRAS G13D specific sensitivity to cetuximab in cellular models, and both have implicated the tumor suppressor NF1 as a critical variable in determining sensitivity and resistance.
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