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Validated All-in-One™ qPCR Primer for TNK2(NM_005781.5) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes a tyrosine kinase that binds Cdc42Hs in its GTP-bound form and inhibits both the intrinsic and GTPase-activating protein (GAP)-stimulated GTPase activity of Cdc42Hs. This binding is mediated by a unique sequence of 47 amino acids C-terminal to an SH3 domain. The protein may be involved in a regulatory mechanism that sustains the GTP-bound active form of Cdc42Hs and which is directly linked to a tyrosine phosphorylation signal transduction pathway. Several alternatively spliced transcript variants have been identified from this gene, but the full-length nature of only two transcript variants has been determined. [provided by RefSeq].
Gene References into function
- ACK-1 and ACK-2 have roles in transducing Cdc42 signals directly to the nucleus
- binding specificity to activated Cdc42-associated kinase is conferred by a specific region in Cdc42
- crystal structures of the human ACK1 kinase domain in both the unphosphorylated and phosphorylated states
- Data show that in the presence of SNX9, synaptojanin-1 is able to colocalize with distinct ACK1 containing vesicles.
- overexpression of Ack1 in cancer cell lines can increase the invasive phenotype of these cells; Ack1 is involved in extracellular matrix-induced integrin signaling, ultimately activating signaling processes like the activation of the small GTPase Rac
- Ack1 promotes prostate tumorigenesis by tyrosine phosphorylation of tumor suppressor Wwox at Tyr-287. It results in polyubiquitination and degradation of Wwox.
- Molecular chaperone heat shock protein 90beta (Hsp90beta)-bound Ack1 and treatment of prostate cells with geldanamycin, a Hsp90 inhibitor, inhibited Ack1 kinase activity and suppressed prostate tumorigenesis.
- Dimerization in response to EGF and activated Cdc42-associated tyrosine kinase 2 (ACK2), which is mediated by the BAR domain, is essential for the intracellular function of SH3PX1.
- These experiments suggest a functional role for Ack as an early transducer of multiple extracellular stimuli.
- The interaction between Ack1 and p130(Cas) occurred through their respective SH3 domains, while the substrate domain of p130(Cas) was the major site of Ack1-dependent phosphorylation.
- The results were confirmed at the level of mRNA and protein, and suggested that four genes (OPCML, RNASE1, YES1 and ACK1) could play a key role in the tumorigenesis and metastasis of gastric cancer.
- Ack1 activated by surface signals or oncogenic mechanisms may directly enhance AR transcriptional function and promote androgen-independent progression of prostate cancer.
- Ack1 promotes prostate cancer progression to androgen-independence via androgen receptor tyrosine phosphorylation at Tyr-267 and Tyr-363, both sites located within the transactivation domain.
- These data suggest that Ack1 is involved in an early step of EGFR desensitization.
- TNK2 enhanced migration and invasion of breast cancer cells by preserving EGFR expression, inspite of its previously reported signalling via BCAR1, explaining its oncogenic behaviour in vitro and correlation with metastatic human breast cancer in vivo.
- These data define Ack1 as a novel interaction partner of nephrocystin-1 and implicate cell-cell junctions and the renal collecting duct in the pathology of nephronophthisis.