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both BIM and BCL2 proteins are regulated by LMTK2 in a GSK3beta- and PP1A-dependent manner.
Mutation of the di-acidic export motif led to endoplasmic reticulum retention of LMTK2, and an increase in protein half-life.
Lemur Tyrosine Kinase-2 (LMTK2), negatively regulates androgen-dependent and androgen-independent prostate cancer cell proliferation. In addition, LMTK2 also negatively regulates the androgen receptor transcriptional activity.
Data indicate that Lemur tyrosine kinase 2 (LMTK2) localizes at the plasma membrane and co-immunoprecipitates with cystic fibrosis transmembrane conductance regulator (CFTR) in airway epithelial cells.
The results indicate that lemur tyrosine kinase 2 is an integral membrane protein in which both the amino and carboxyl termini are exposed to the cytoplasm. Moreover, this topology places the kinase active site within the cytoplasm.
We describe a new signalling pathway within the nervous system that links cdk5/p35 with phosphatase-1C and which has implications for a number of neuronal functions and neuronal dysfunction
Low LMTK2 expression is associated with the development of prostate cancer.
Data show that downregulation of myosin VI expression results in a significant reduction in PSA and VEGF secretion in LNCaP cells, and the intracellular targeting seems to involve myosin VI-interacting proteins, GIPC and LMTK2 and Dab2.
KPI-2 is a kinase with sites to associate with PP1C and Inh2 to form a regulatory complex that is localized to membranes
Cprk is expressed in a number of tissues but is enriched in brain and muscle; Cprk displays catalytic activity in kinase assays and is itself phosphorylated by cdk5/p35; Cdk5/p35 inhibits cprk activity
BREK, Brain Enriched Kinase, is a new member of the family of protein serine/threonine kinases; plays important roles in NGF-TrkA signalling in the brain [BREK]
role of the segment KLHY in binding with protein phosphatase 1
Myosin VI and LMTK2 are required for the transport of cargo, such as the Transferrin Receptor, from early endosomes to the endocytic recycling compartment.
Results show that BREK is critical for the transition of endocytosed membrane vesicles from early endosomes to recycling endosomes and also suggest an involvement of myosin VI in this pathway.
The protein encoded by this gene belongs to the protein kinase superfamily and the protein tyrosine kinase family. It contains N-terminal transmembrane helices and a long C-terminal cytoplasmic tail with serine/threonine/tyrosine kinase activity. This protein interacts with several other proteins, such as Inhibitor-2 (Inh2), protein phosphatase-1 (PP1C), p35, and myosin VI. It phosporylates other proteins, and is itself also phosporylated when interacting with cyclin-dependent kinase 5 (cdk5)/p35 complex. This protein involves in nerve growth factor (NGF)-TrkA signalling, and also plays a critical role in endosomal membrane trafficking. Mouse studies suggested an essential role of this protein in spermatogenesis.
, apoptosis-associated tyrosine kinase 2
, brain-enriched kinase
, cyclin-dependent kinase 5/p35-regulated kinase
, kinase phosphatase inhibitor 2
, kinase/phosphatase/inhibitor 2
, serine/threonine-protein kinase KPI-2
, serine/threonine-protein kinase LMTK2