Sentence examples for mutations in receptor from inspiring English sources

These issues are also critical when interpreting structure function studies of allosteric GPCR modulators because mutations in receptor structure, either engineered or naturally occurring, can differentially affect not only modulator affinity, but also the nature, magnitude and direction of the allosteric effect on orthosteric ligand function.

AML is associated with a wide range of genetic alterations, including mutations in receptor tyrosine kinases (RTKs) that perturb intracellular signaling networks which play a role in leukemia pathogenesis and are manifested in the clinical heterogeneity of the disease.

These efforts also recognize the need to address the widespread problem of emerging resistance to current drugs, including frequent gatekeeper mutations in receptor tyrosine kinases.

It has been suggested that second mutations, such as activating point mutations, in receptor tyrosine kinases (e.g., FLT3 and c-KIT) are required for fusion genes such as AML1-ETO, PML-RARa, or CBFb-MYH11 to induce acute leukemia.

Together with the previously discussed activity-related mislocalisation observed for oncogenic Kit mutants the present study completes the picture that aberrant intracellular signalling is a general characteristic of GISTs that harbour mutations in receptor tyrosine kinases (KIT or PDGFRα).

We describe an increased rate of mutations in receptor tyrosine kinases (RTKs) and associated signaling effectors, for example, in EGFR, ERBB3, KRAS and MAP2K2, pointing to a role of aberrant RTK signaling in the development or progression of MM.

Moreover, drug receptors are also encoded by polymorphic genes [ 39] and mutations in receptors, such as the receptor tyrosine kinases, have been linked to various cancers and neurodegenerative diseases [ 41- 44].

The number of tumours (particularly squamous cell carcinomas) containing GTP-bound Ras is however much higher, likely owing to the autocrine/paracrine activation and/or to mutation in receptor tyrosine kinases such as the EGFR (Khavari and Rinn, 2007).

The mutation positions found in the donor tract are imported to the receptor, and the mutations in the receptor tract are erased.

Over 40 missense mutations in TNF receptor 1 (theR1), the prototypical proinflammatory receptor, have been associated with TRAPS.

These cancers are often correlated with receptor over-expression and/or mutations in the receptor tyrosine kinase, frequently associated with poor prognosis for patients [ 2].