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Validated All-in-One™ qPCR Primer for MAP3K14(NM_003954.3) Search again
By 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.
Validated result:
Summary
This gene encodes mitogen-activated protein kinase kinase kinase 14, which is a serine/threonine protein-kinase. This kinase binds to TRAF2 and stimulates NF-kappaB activity. It shares sequence similarity with several other MAPKK kinases. It participates in an NF-kappaB-inducing signalling cascade common to receptors of the tumour-necrosis/nerve-growth factor (TNF/NGF) family and to the interleukin-1 type-I receptor. [provided by RefSeq].
Gene References into function
- results demonstrate that IKK2 is essential for dendritic cell activation induced by CD40L or contact with allogeneic T cells, but not by LPS, whereas NIK is not required for any of these signals
- induction of noncanonical NF-kappaB signaling may involve the rescue of NIK from TRAF3-mediated negative regulation
- subcellular distribution of NIK to different compartments might be a means of regulating the function of this kinase
- Results for the first time place NF-kappa B-inducing kinase (NIK), previously shown to function in TNF signaling, within the interferon signal transduction pathway
- in addition to activating NF-kappaB/p52, LIGHT also activates Stat3 through the NIK pathway
- This study demonstrates that NF-kappaB-inducing kinase (NIK) is a critical target of the endogenous ROS in NF-kappaB pathways.
- NF-kappaB-inducing kinase phosphorylates and blocks the degradation of Down syndrome candidate region 1
- NIK functions downstream of Cot to mediate p65 phosphorylation.
- Translocation of NF-kappa B to the nucleus in prostatic cancer might be due to overexpression of several components of the NIK pathway.
