Sentence examples for mutations of receptor from inspiring English sources

Overexpression and activating mutations of receptor tyrosine kinases (RTKs) are known to be involved in the pathogenesis of many types of cancer.

PCC/PGL can be broadly divided into a pseudohypoxic cluster and tumours mutations of receptor tyrosine kinase signalling.

Mutations of receptor tyrosine kinases (FLT3 and KIT), commonly seen in de novo AML, are infrequent in MDS.

Laboratory analyses of snap-frozen tumour tissues were performed to detect activation and genetic mutations of receptor tyrosine kinases (RTKs) in TC samples.

Even though mutations of receptor or kinase domain genes have been identified as the major reason of resistance to other targeted therapies such as ACR-ABL and EGFR inhibitors, this is not the case in VEGF-targeted drug resistance.

Based on the identification of residues that determine receptor selectivity in arrestins and the phylogenetic analysis of the arrestin (arr) family, we introduced fifteen mutations of receptor-discriminator residues in arr-3, which were identified previously using mutagenesis, in vitro binding, and BRET-based recruitment assay in intact cells.

This observation indicates that, although resistance development can occur through various mechanisms (deletion or mutation of receptor sites, host DNases,.), modification or loss of the EPS receptor must be the most straightforward.

Previous studies have shown that mutation of receptor tyrosine residues to phenylalanine (such as in our Tie2 mutants) can affect kinase activity of the receptor.

Two decades of molecular studies have identified important genetic events such as dysregulation of growth factor signaling via amplification or mutation of receptor tyrosine kinase genes; activation of PI3K pathway; and inactivation of p53 and Rb tumor suppressor pathways [ 2].

Objective: To search for somatic activating mutations of gonadotropin receptor (FSH-R and LH/chorionic gonadotropin receptor [CG-R]) genes as a cause of sex cord stromal tumors.

X-linked congenital nephrogenic diabetes insipidus (cNDI) has thus been described as a loss of function of the vasopressin (AVP) V2 receptor, and more than 200 mutations of the receptor gene have been identified [2].