Cdk9, a member of the cdc2-like family of kinases, binds to gp130, the receptor of the IL-6 family of cytokines

Flavopiridol induces phosphorylation of AKT in a human glioblastoma cell line, in contrast to siRNA-mediated silencing of Cdk9: Implications for drug design and development

“…5,22,30,[35][36][37] It was observed that one of the cellular functions of the Cdk9 and cyclins T complex consists of protecting cells from apoptosis in normal tissues. 5,23,38 It was also reported that the Cdk9 pathway has the ability to promote the expression of anti-apoptotic factors, such as myeloid cell leukemia 1 (MCL-1). 5,28,39,40 Dysfunctions in the anti-apoptotic signaling system of the Cdk9-related pathway may lead to carcinogenesis, as reported in a variety of other systems, such as the axis of the insulin-like growth factor-I receptor (IGF-1R), autocrine/paracrine secreted Frizzled-related protein 2, has different status for p53 expression ( Table 1).…”

“…[1][2][3][4][5][6][21][22][23][24][25][26][27][28][29][30][31][32][33][34] For instance, the Cdk9-interacting cellular factors comprise MyoD, retinoblastoma protein (pRb), p53, c-Myc, hSPT5 and gp130. 5 In these cases, the Cdk9-related pathway controls the phosphorylation of the aforementioned cellular factors.…”

Cyclin T1 overexpression induces malignant transformation and tumor growth

“…14,16,17,[30][31][32][33] For instance, one of the functions of CDK9 and its Cyclin partners consists of protecting cells from apoptotic injuries in normal tissues. 34,35 In this context, CDK9 and type T cyclins may promote the expression of anti-apoptotic factors such as myeloid cell leukemia 1 (MCL-1). 12,36,37 A deregulation in the antiapoptotic CDK9-signaling system may lead to malignant cell transformation, as reported in a number of other systems, such as insulin-like growth factor-I receptor, epidermal growth factor receptor, autocrine/ paracrine secreted Frizzled-related protein 2, AKTrelated pathway and surviving.…”

Flavopiridol Protects Against Inflammation by Attenuating Leukocyte-Endothelial Interaction via Inhibition of Cyclin-Dependent Kinase 9

“…On the basis of a few studies, CDK9 inhibition was thought to be of potential value to fight inflammation. Independent of its function as a subunit of P-TEFb, CDK9 was found to interact with cytoplasmic regions of gp130, 24 the receptor for the proinflammatory cytokine IL-6. An additional study reported that CDK9 inhibitors disrupt the IL-6/STAT3 signaling in the liver.…”