anti-MAP3K14 (MAP3K14) 抗体产品概述

Human Mitogen-Activated Protein Kinase Kinase Kinase 14 (MAP3K14) interaction partners

1. 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 (显示 CRMP1 抗体).

2. results suggest that changes in the relative concentrations of RelB (显示 RELB 抗体), NIK:IKK1, and p100 (显示 CUX1 抗体) during noncanonical signaling modulate this transitional complex and are critical for maintaining the fine balance between the processing and protection of p100 (显示 CUX1 抗体).

3. report a detailed state-of-the-art mass spectrometry-based protein-protein interaction network including the noncanonical NF-kappaB (显示 NFKB1 抗体) signaling nodes TRAF2 (显示 TRAF2 抗体), TRAF3 (显示 TRAF3 抗体), IKKalpha (显示 CHUK 抗体), NIK, and NF-kappaB2/p100 (显示 CUX1 抗体); also provide a differential interactome of NIK mutants that cause immunodeficiency

4. OLFM1 (显示 OLFM1 抗体) is a negative regulator of non-canonical NF-kappaB (显示 NFKB1 抗体) signalling by interacting with and inhibiting NIK. Thus, OLFM1 (显示 OLFM1 抗体) may serve as a valuable biomarker and therapeutic target for colorectal cancer (CRC (显示 CALR 抗体)) patients.

5. The expression of OTUD7B (显示 OTUD7B 抗体) 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 (显示 ODZ1 抗体) stage. high OTUD7B (显示 OTUD7B 抗体)/low NIK index can predict an good prognosis.

6. 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.

7. This study identified two novel independent loci (MAP3K14 and CARD9 (显示 CARD9 抗体)) strongly associated with joint damage in Mexican Americans and European Americans and a few shared loci showing suggestive evidence for association.

8. The forced expression of NDRG2 (显示 NDRG2 抗体) in ATL cells down-regulates not only the canonical pathway by inhibiting AKT (显示 AKT1 抗体) signaling but also the non-canonical pathway by inducing NF-kappaB (显示 NFKB1 抗体)-inducing kinase (NIK) dephosphorylation via the recruitment of PP2A (显示 PPP2R4 抗体)

9. NIK(+) endothelial cells may play an important role in the persistence of synovitis

10. Data suggest microRNA302c, but not microRNA520e, promotes replication of influenza A virus H3N2 although the two microRNAs target same site of NFkappaB (显示 NFKB1 抗体)-inducing kinase (MAP3K14) 3prime untranslated region; studies were conducted in lung epithelial cells.

Mouse (Murine) Mitogen-Activated Protein Kinase Kinase Kinase 14 (MAP3K14) interaction partners

1. global or thymus-specific ablation of the NIK (显示 MAP4K4 抗体) gene results in fatal autoimmune liver disease in mice.

2. These findings highlight the importance of NIK (显示 MAP4K4 抗体) in tumor pathogenesis and invite new therapeutic strategies that attenuate mitochondrial dysfunction through inhibition of NIK (显示 MAP4K4 抗体) and Drp1 (显示 CRMP1 抗体).

3. constitutive activation of NIK (显示 MAP4K4 抗体) in the hematopoietic system leads to bone marrow (BM) failure and postnatal lethality.

4. results suggest that changes in the relative concentrations of RelB (显示 RELB 抗体), NIK:IKK1, and p100 (显示 PATL2 抗体) during noncanonical signaling modulate this transitional complex and are critical for maintaining the fine balance between the processing and protection of p100 (显示 PATL2 抗体).

5. NIK (显示 MAP4K4 抗体) pathways in both hepatocytes and immune cells act in concert to promote liver steatosis and glucose production in the setting of obesity.

6. this study demonstrates that although NIK (显示 MAP4K4 抗体) is dispensable for thymocyte development, it has a cell-intrinsic role in regulating the homeostasis and function of peripheral T cells

7. Using a novel conditional mutant of NIK (显示 MAP4K4 抗体), the authors could show in vivo that NIK (显示 MAP4K4 抗体) signaling in thymic epithelial cells is essential for the thymic hardwiring of gammadelta T cell cytokine production.

8. NIK (显示 MAP4K4 抗体) not only contributes to lymphoid organogenesis, inflammation and cell survival but also to TNFR1 (显示 TNFRSF1A 抗体)/RIP1 (显示 RALBP1 抗体)-dependent cell death independently of the alternative NF-kappaB (显示 NFKB1 抗体) pathway.

9. This study demonstrated that NFkappaB-inducing kinase inhibits NFkappaB activity specifically in neurons of the CNS.

10. results assign NIK (显示 MAP4K4 抗体)-induced alternative NF-kappaB (显示 NFKB1 抗体) 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