Protein Changes Function in Mutated Cells
By Biotechdaily staff writers
Posted on 29 Nov 2004
Researchers have found that a protein activated by Kit, a mast cell membrane tyrosine kinase receptor required for normal blood cell formation and development, functions differently depending on whether it is present in normal or cancerous tissue.Posted on 29 Nov 2004
Investigators at the U.S. National Cancer Institute (Bethesda, MD, USA) worked with cell cultures of normal (wild type) mouse mast cells and a mutated line where the gene for Kit miscoded an aspartic acid residue. In particular they looked at the consequences of Kit binding to protein kinase delta (PKCdelta), a protein involved in cell signaling. They found that inhibition of PKCdelta reduced the growth of the mutant mouse mast cell line by approximately 40%, while the growth of normal mast cells was not affected. These findings were published in the November 12, 2004, online edition of Blood.
"This work is a promising study on cancer inhibition,” said senior author Dr. Diana Linnekin, a researcher at the [U.S.] National Cancer Institute. "This is the first demonstration of a function change in PKCdelta resulting from an oncogenic mutation in a growth factor receptor.”
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