TK+

(redirected from Tyrosine Kinase Domain)
AcronymDefinition
TK+Tyrosine Kinase Domain
TK+thymidine kinase positive
TK+thymidine kinase competent
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References in periodicals archive ?
The cytoplasmic region of the [beta]-subunit consists of several functional domains including a juxtamembrane region, a tyrosine kinase domain and the carboxy-terminal-region (5,11).
(24) Interestingly, the amino acid sequence of ROS1 and ALK is similar within the tyrosine kinase domains, and the crizotinib binding site is nearly identical.
Gale, "FLT3 tyrosine kinase domain mutations are biologically distinct from and have a significantly more favorable prognosis than FLT3 internal tandem duplications in patients with acute myeloid leukemia," Blood, vol.
The activation of EGFR may be inhibited by a number of mechanisms including antibody therapy directed against the extracellular ligand binding domain and small molecule inhibitors targeting the intracellular tyrosine kinase domain. The side effect profile and therapeutic window of the antibody agents and tyrosine kinase inhibitors (TKIs) differ, as does their clinical activity, across different gastrointestinal tumour types.
According to the company, gilteritinib is an investigational compound that has demonstrated inhibitory activity against FLT3 internal tandem duplication (ITD) as well as FLT3 tyrosine kinase domain (TKD), two common types of FLT3 mutations seen in one-third of patients with AML.
(9) Small-molecule inhibitors designed to block the adenosine triphosphate (ATP)-binding groove in the EGFR tyrosine kinase domain appeared to effectively kill lung ACA cells in vitro and showed promise in early clinical studies.
Furthermore, there are three small-molecule inhibitors of the tyrosine kinase domain (TKIs) that interfere with the binding of ATP, also approved to treat non-small cell lung cancer (i.e., gefitinib, erlotinib, and lapatinib) [4].
Each receptor consists of an intracellular tyrosine kinase domain, a transmembrane domain and an extracellular ligand-binding domain.
Gilteritinib has demonstrated inhibitory activity against FLT3 internal tandem duplication as well as FLT3 tyrosine kinase domain, two common types of FLT3 mutations seen in patients with AML.
Epidermal Growth Factor Receptor.--Recognized mechanisms of epidermal growth factor receptor (EGFR) gain of function in non-small cell lung carcinoma (NSCLC) include somatic activating mutations in the exons encoding the tyrosine kinase domain and EGFR gene amplification.
These receptors are all composed of an extracellular ligand-binding domain, a transmembrane lipophilic domain, and an intracellular tyrosine kinase domain and, with the exception of HER2, all bind to receptor-specific ligands (Figure 1).
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