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Germinal center kinases (GCKs), such as TNIK, are characterized by an N-terminal kinase domain and a C-terminal GCK domain that serves a regulatory function (Fu et al., 1999 [PubMed 10521462]).[supplied by OMIM, Mar 2008].. Additionally we are shipping TNIK Antibodies (163) and TNIK Kits (2) and many more products for this protein.
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results provide new evidence that TNIK may be involved in the proliferation of multiple myeloma IM-9 cells and in the anti-cancer activity of dovitinib via inhibition of the endogenous Wnt (show WNT2 Proteins) signaling pathway.
Exome sequencing of the index in each family revealed the same homozygous truncating mutation in TNIK that results in complete loss of the protein. TNIK is a kinase with a well-established role in dendrite development and synaptic transmission. The phenotype we observe in human patients who lack TNIK is consistent with the previously published Tnik (-/-) phenotype in the murine model
Here we present the result of a 4-stage genome-wide association study composed of 5,953 adolescent idiopathic scoliosis patients and 8,137 controls. Overall, we identified three novel susceptible loci including rs7593846 at 2p14 near MEIS1 (show MEIS1 Proteins) , rs7633294 at 3p14.1 near MAGI1 (show MAGI1 Proteins) and rs9810566 at 3q26.2 near TNIK
Our results demonstrated that TNIK might play a crucial role in pancreatic carcinogenesis and serve as a novel therapeutic target of pancreatic cancer.
High expression of TNIK in colorectal cancer was associated with recurrence in stage II and III colorectal cancer patients.
Endogenous substrates of TNIK were identified in neurons, along with consensus sequences for TNIK.
nuclear p-TNIK expression was studied in hepatocellular carcinoma, and p-TNIK nuclear expression was associated with poor prognosis and is a candidate prognostic marker for hepatocellular carcinoma
Dynamic change of TNIK offers a way to protect cells from outside stimulus.
TNIK mediates proliferation and survival of EBV-transformed B-cells.
TNIK is essential for the activation of both the canonical Wnt (show WNT2 Proteins) pathway and the JNK (show MAPK8 Proteins) pathway, and serves as a pro-survival factor.
This study demonstrate here that TNIK is expressed in neurons throughout the adult mouse brain.
TNiK is required for dentate gyrus neurogenesis & for pattern separation in a 2-choice spatial discrimination task & for glutamate (show GRIN1 Proteins)-dependent object-location paired associate learning.
TNIK maintains levels of glutamate receptors and other key postsynaptic density (PSD) proteins at the synapse, with loss of TNIK protein or inhibition of TNIK activity causing rapid degradation of PSD constituents.
siRNA depletion of TNIK followed by expression array analysis showed that TNIK is an essential, specific activator of Wnt (show WNT2 Proteins) transcriptional programme.
Germinal center kinases (GCKs), such as TNIK, are characterized by an N-terminal kinase domain and a C-terminal GCK domain that serves a regulatory function (Fu et al., 1999
TRAF2 and NCK interacting kinase
, TRAF2 and NCK-interacting protein kinase-like
, TRAF2 and NCK-interacting protein kinase
, traf2 and NCK-interacting protein kinase
, Traf2 and NCK interacting kinase