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These findings highlight the importance of NIK in tumor pathogenesis and invite new therapeutic strategies that attenuate mitochondrial dysfunction through inhibition of NIK and Drp1.
results suggest that changes in the relative concentrations of RelB (show RELB Proteins), NIK:IKK1, and p100 (show CUX1 Proteins) during noncanonical signaling modulate this transitional complex and are critical for maintaining the fine balance between the processing and protection of p100 (show CUX1 Proteins).
report a detailed state-of-the-art mass spectrometry-based protein-protein interaction network including the noncanonical NF-kappaB (show NFKB1 Proteins) signaling nodes TRAF2 (show TRAF2 Proteins), TRAF3 (show TRAF3 Proteins), IKKalpha (show CHUK Proteins), NIK, and NF-kappaB2/p100 (show CUX1 Proteins); also provide a differential interactome of NIK mutants that cause immunodeficiency
OLFM1 (show OLFM1 Proteins) is a negative regulator of non-canonical NF-kappaB (show NFKB1 Proteins) signalling by interacting with and inhibiting NIK. Thus, OLFM1 (show OLFM1 Proteins) may serve as a valuable biomarker and therapeutic target for colorectal cancer (CRC (show CALR Proteins)) patients.
The expression of OTUD7B (show OTUD7B Proteins) and NIK were negatively correlated in non-small cell lung cancer tumor samples. the higher expression of NIK was related to more lymph node metastasis and later TNM (show ODZ1 Proteins) stage. high OTUD7B (show OTUD7B Proteins)/low NIK index can predict an good prognosis.
NIK expression was significantly increased in the tumor tissue of patients with breast carcinoma, which may be an important factor that affects the prognosis of these patients.
This study identified two novel independent loci (MAP3K14 and CARD9 (show CARD9 Proteins)) strongly associated with joint damage in Mexican Americans and European Americans and a few shared loci showing suggestive evidence for association.
The forced expression of NDRG2 (show NDRG2 Proteins) in ATL cells down-regulates not only the canonical pathway by inhibiting AKT (show AKT1 Proteins) signaling but also the non-canonical pathway by inducing NF-kappaB (show NFKB1 Proteins)-inducing kinase (NIK) dephosphorylation via the recruitment of PP2A (show PPP2R4 Proteins)
NIK(+) endothelial cells may play an important role in the persistence of synovitis
Data suggest microRNA302c, but not microRNA520e, promotes replication of influenza A virus H3N2 although the two microRNAs target same site of NFkappaB (show NFKB1 Proteins)-inducing kinase (MAP3K14) 3prime untranslated region; studies were conducted in lung epithelial cells.
constitutive activation of NIK (show MAP4K4 Proteins) in the hematopoietic system leads to bone marrow (BM) failure and postnatal lethality.
results suggest that changes in the relative concentrations of RelB (show RELB Proteins), NIK:IKK1, and p100 (show PATL2 Proteins) during noncanonical signaling modulate this transitional complex and are critical for maintaining the fine balance between the processing and protection of p100 (show PATL2 Proteins).
NIK (show MAP4K4 Proteins) pathways in both hepatocytes and immune cells act in concert to promote liver steatosis and glucose production in the setting of obesity.
this study demonstrates that although NIK (show MAP4K4 Proteins) is dispensable for thymocyte development, it has a cell-intrinsic role in regulating the homeostasis and function of peripheral T cells
Using a novel conditional mutant of NIK (show MAP4K4 Proteins), the authors could show in vivo that NIK (show MAP4K4 Proteins) signaling in thymic epithelial cells is essential for the thymic hardwiring of gammadelta T cell cytokine production.
NIK (show MAP4K4 Proteins) not only contributes to lymphoid organogenesis, inflammation and cell survival but also to TNFR1 (show TNFRSF1A Proteins)/RIP1 (show RALBP1 Proteins)-dependent cell death independently of the alternative NF-kappaB (show NFKB1 Proteins) pathway.
This study demonstrated that NFkappaB-inducing kinase inhibits NFkappaB activity specifically in neurons of the CNS.
results assign NIK (show MAP4K4 Proteins)-induced alternative NF-kappaB (show NFKB1 Proteins) signaling a master regulatory role in B-cells, starting from the T1 stage and also show that B-1 B cells are less dependent on this pathway, presumably owing to the existence of alternative pathways yet to be determined
NIK (show MAP4K4 Proteins), and thus probably the noncanonical NF-kappaB (show NFKB1 Proteins) pathway, is critical to allow DCs to acquire the capacity to cross-present antigen and prime CD8 (show CD8A Proteins) T cells after exposure to licensing stimuli.
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.
, serine/threonine protein-kinase
, serine/threonine-protein kinase NIK
, NF kappa B-inducing kinase
, Nfkb inducing kinase
, protein kinase
, mitogen-activated protein kinase kinase kinase 14