anti-MAP3K14 (MAP3K14) 抗体产品概述

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

1. findings identify a NIK-SIX signalling axis that fine-tunes inflammatory gene expression programs under both physiological and pathological conditions

2. Molecular dynamics simulations were employed to differentiate the structural dynamics of the NF-kappaB Inducing Kinase (NIK), a protein kinase responsible for invoking the non-canonical NF-kappaB pathway, in its native and mutant form, and in the absence and presence of salt concentration in efforts to probe whether changes in the ionic environment stabilize or destabilize the NIK dimer

3. we identify nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB)-inducing kinase (NIK) as a potential drug target driving NF-kappaB signaling and Merlin-deficient schwannoma genesis

4. Results indicated that MAP3K14 is a susceptibility gene for leprosy.

5. A TRAF3-NIK axis differentially regulates viral DNA vs RNA pathways in innate immune signaling.

6. Data show that breast cancer stem cells (BCSCs) expressed higher levels of NF-kappaB-inducing kinase (NIK).

7. 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.

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

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

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

11. The expression of OTUD7B 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 stage. high OTUD7B/low NIK index can predict an good prognosis.

12. 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.

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

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

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

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

17. TWEAK induces noncanonical NF-kappaB signaling and signal-specific regulation of NIK mRNA expression.

18. by demonstrating a critical role of NIK in mediating NF-kappaB activation and BAG3 induction upon ST80/Bortezomib cotreatment, our study provides novel insights into mechanisms of resistance to proteotoxic stress in RMS

19. Loss-of-function mutations in NIK can cause B-cell lymphopenia, hypogammaglobulinemia, impaired ICOSL expression, and disordered T helper cell and NK cell function.

20. Membrane attack complexes activate noncanonical NF-kappaB by forming a novel Akt(+)NIK(+) signalosome on Rab5(+) endosomes.

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

1. NIK is an essential post-transcriptional regulator of T-cell activation affecting F-actin dynamics and TCR signaling.

2. The authors demonstrated that miR-23b mediated immunosuppression during late sepsis by inhibiting the noncanonical NF-kappaB signal and promoting the proapoptotic signal pathway by targeting NIK, TRAF1, and XIAP.

3. Islet alpha-cell specific overexpression of NIK results in islet alpha-cell dysfunction and causes islet beta-cell death and pancreatitis, which are most likely due to paracrine secretion of cytokines and chemokines from islet alpha cells, thus leading to hypoglycemia, growth retardation, and postnatal death in mice.

4. our data suggest a pivotal role for the NIK signaling axis in regulating dendritic cell functions in intestinal immunity and homeostasis.

5. A TRAF3-NIK axis differentially regulates viral DNA vs RNA pathways in innate immune signaling.

6. Pathological activation of hepatic NIK likely blocks hepatocyte replication, contributing to liver disease progression.

7. Nik(-/-) mice could be useful as a spontaneous model of specific features of Eosinophilic esophagitis.

8. global or thymus-specific ablation of the NIK gene results in fatal autoimmune liver disease in mice.

9. 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.

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

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

12. NIK pathways in both hepatocytes and immune cells act in concert to promote liver steatosis and glucose production in the setting of obesity.

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

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

15. NIK not only contributes to lymphoid organogenesis, inflammation and cell survival but also to TNFR1/RIP1-dependent cell death independently of the alternative NF-kappaB pathway.

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

17. results assign NIK-induced alternative NF-kappaB 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

18. NIK, and thus probably the noncanonical NF-kappaB pathway, is critical to allow DCs to acquire the capacity to cross-present antigen and prime CD8 T cells after exposure to licensing stimuli.

19. Deletion of NIK in adult mice results in decreases in B cell populations in lymph nodes and spleen, similar to what is observed upon blockade of BAFF.

20. We identify NIK as a critical negative regulator of beta cell function, as pharmacological NIK activation results in impaired glucose-stimulated insulin secretion in mouse and human islets.