TESK1 — Testis associated actin remodelling kinase 1
TESK1 belongs to a gene co-expression module in 2 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.
TESK1's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Macrophages | ER Stress UPR Stress | ANKRD9, APEH, ARMCX6, BET1L, CALR, CCDC107, COPS2, DNAJB11 +20 more | View in SCUBA |
| Mucosal-associated invariant T cell | Polycomb Repression DNA/chromatin regulation | BTBD6, CBX4, CD81, CSNK1G2, CTBP1, DUS1L, GNB1, GRK6 +15 more |
About the gene
| Chromosome | 9: 35605262-35610041 |
|---|---|
| Predicted location | Intracellular |
| Essential gene | No |
| Protein class | Enzymes, Plasma proteins, Predicted intracellular proteins |
| Molecular function | Kinase, Serine/threonine-protein kinase, Transferase, Tyrosine-protein kinase |
Function
Dual specificity protein kinase activity catalyzing autophosphorylation and phosphorylation of exogenous substrates on both serine/threonine and tyrosine residues (By similarity). Regulates the cellular cytoskeleton by enhancing actin stress fiber formation via phosphorylation of cofilin and by preventing microtubule breakdown via inhibition of TAOK1/MARKK kinase activity (By similarity). Inhibits podocyte motility via regulation of actin cytoskeletal dynamics and phosphorylation of CFL1 (By similarity). Positively regulates integrin- mediated cell spreading, via phosphorylation of cofilin. Suppresses ciliogenesis via multiple pathways; phosphorylation of CFL1, suppression of ciliary vesicle directional trafficking to the ciliary base, and by facilitating YAP1 nuclear localization where it acts as a transcriptional corepressor of the TEAD4 target genes AURKA and PLK1. Probably plays a central role at and after the meiotic phase of spermatogenesis (By similarity).
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.