CDK9-Cyclin T
Cyclin-dependent kinases (CDKs) are proteins pivotal to a wide range of cellular functions,
most importantly cell division and transcription, and their dysregulations have been
implicated as prominent drivers of tumorigenesis
most importantly cell division and transcription, and their dysregulations have been
implicated as prominent drivers of tumorigenesis
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Adenosine Triphosphate (ATP) Binding Motif forms a cleft between the N- and C-terminal lobes and is highly conserved among CDKs
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The major cyclin partner of CDK9, cyclin T (‘T’ named after the first letter of HIV TAT), has a close similarity to cyclin C and cyclin H. HIV TAT interacts only with cyclin T1 in complex with CDK9 to mediate HIV transcription
CDK9-cyclin T2a interacts directly with
myoblast determination protein 1 (MyoD)
CDK9-cyclin T1 activates muscle
differentiation programs by stimulating the transcription
program of myocyte enhancer factor 2 [MEF2]
CDK9-cyclin T1 is also required for the differentiation of monocytes, lymphocytes, adipocytes, and neurons.
myoblast determination protein 1 (MyoD)
CDK9-cyclin T1 activates muscle
differentiation programs by stimulating the transcription
program of myocyte enhancer factor 2 [MEF2]
CDK9-cyclin T1 is also required for the differentiation of monocytes, lymphocytes, adipocytes, and neurons.
