V-Maf Musculoaponeurotic Fibrosarcoma Oncogene Family, Protein K (Avian) (MAFK) ELISA Kits

Human V-Maf Musculoaponeurotic Fibrosarcoma Oncogene Family, Protein K (Avian) (MAFK) interaction partners

1. MAFK genetic polymorphisms are significantly associated with susceptibility to ulcerative colitis development in Japan.

2. Findings suggest that MAFK and its target gene GPNMB play important roles in the malignant progression of triple-negative breast cancer (TNBC) cells, offering potentially new therapeutic targets for TNBC patients.

3. Results suggested that Wnt1-induced MAFK expression promoted cell proliferation in MG63 cells, and that the role of MAFK in osteosarcoma might be closely linked to the Wnt signaling pathway.

4. MafK mediated p65 acetylation by CBP upon LPS stimulation, thereby facilitating recruitment of p65 to NF-kappaB promoters such as IL-8 and TNFalpha.

5. Results suggest that JDP2 is an integral component of the Nrf2-MafK complex and that it modulates antioxidant and detoxification programs by acting via the ARE.

6. Data indicate that transcription factors MafK and Bach1 regulate expression of heme oxygenase-1 (HO-1).

7. These findings demonstrate that a combination of p45NF-E2, Maf G, and Maf K is a key determinant of both megakaryopoiesis and thrombopoiesis.

Mouse (Murine) V-Maf Musculoaponeurotic Fibrosarcoma Oncogene Family, Protein K (Avian) (MAFK) interaction partners

1. beta-Cell-Specific Mafk Overexpression Impairs Pancreatic Endocrine Cell Development

2. These data identify Mafg and Mafk as new cataract-associated candidates and define their function in regulating largely non-crystallin genes linked to human cataract.

3. KAP-1 may contribute to the repression of Ey and beta-major globin gene transcription through recruitment to the promoters of these two genes, mediated by the interaction of KAP-1 with either Zfp445 or MafK, respectively

4. These findings demonstrate that a combination of p45NF-E2, Maf G, and Maf K is a key determinant of both megakaryopoiesis and thrombopoiesis.

5. MafF, MafG, and MafK triple-knockout mice developed normally until embryonic day 9.5 (E9.5). Thereafter, however, the triple-knockout embryos showed severe growth retardation and liver hypoplasia, and the embryos died around E13.5.

6. Thus compound mafG::mafK mutants develop age- and maf gene dosage-dependent cell-autonomous neuronal deficiencies that lead to profound neurological defects.

7. regulation of dynamic exchange with Bach1

8. mafG::mafK::mafF triple-mutant fibroblasts that completely lack small Mafs are highly susceptible to oxidative stress. (mafK)

9. DNA-binding activity of endogenous MafA was significantly increased in the MafK transgenic mice

10. The involvement of both HNF4alpha and NF-E2 in Abcc6 gene regulation suggests that Abcc6 might be involved in a detoxification processes related to hemoglobin or heme.

11. MafK/NF-E2 p18 recruitment was involved in the physical proximity of LCR and active beta-globin genes upon beta-globin gene transcriptional activation.

12. Histological analysis revealed that embryonic development of beta cells in the MafA(-/-)MafK(+) mice was significantly suppressed and the reduced number of beta cells was responsible for the early onset of diabetes.