| Inhibition of HMOX1 by MAFG potentiates the development of depression-like behavior in mice associated with astrocyte-mediated neuroinflammation. | Inhibition of HMOX1 by MAFG potentiates the development of depression‑like behavior in mice associated with astrocyte-mediated neuroinflammation.
Ye Y, Liang J, Xu C, Liu Y, Chen J, Zhu Y. | 08/30/2024 |
| Silencing Mafg in mouse hepatocytes and obese mice elicits a fasting-like gene expression profile, improves glucose metabolism. | A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism.
Pradas-Juni M, Hansmeier NR, Link JC, Schmidt E, Larsen BD, Klemm P, Meola N, Topel H, Loureiro R, Dhaouadi I, Kiefer CA, Schwarzer R, Khani S, Oliverio M, Awazawa M, Frommolt P, Heeren J, Scheja L, Heine M, Dieterich C, Büning H, Yang L, Cao H, Jesus DF, Kulkarni RN, Zevnik B, Tröder SE, Knippschild U, Edwards PA, Lee RG, Yamamoto M, Ulitsky I, Fernandez-Rebollo E, Vallim TQA, Kornfeld JW., Free PMC Article | 05/16/2020 |
| results provide direct evidence that the Nrf2-MafG heterodimer acts as a transcriptional activator of Nrf2-dependent genes | Direct and Specific Functional Evaluation of the Nrf2 and MafG Heterodimer by Introducing a Tethered Dimer into Small Maf-Deficient Cells.
Katsuoka F, Otsuki A, Takahashi M, Ito S, Yamamoto M., Free PMC Article | 03/21/2020 |
| In condition of hypoxia, MAFG induction correlated with reduced levels of miR-128. This lead to increased mRNA levels of HMOX-1 and x-CT for blunting stress. Overall, these findings identify MAFG as novel direct target of miR-128. | miR-128 Is Implicated in Stress Responses by Targeting MAFG in Skeletal Muscle Cells.
Caggiano R, Cattaneo F, Moltedo O, Esposito G, Perrino C, Trimarco B, Ammendola R, Faraonio R., Free PMC Article | 07/21/2018 |
| The CNC-sMaf binding element is strictly required for the Nrf2-sMaf heterodimer function in cytoprotection. | Unique cistrome defined as CsMBE is strictly required for Nrf2-sMaf heterodimer function in cytoprotection.
Otsuki A, Suzuki M, Katsuoka F, Tsuchida K, Suda H, Morita M, Shimizu R, Yamamoto M. | 12/17/2016 |
| The MafG as an FXR target gene and show that hepatic MAFG expression represses genes of the bile acid synthetic pathway and modifies the biliary bile acid composition. | MAFG is a transcriptional repressor of bile acid synthesis and metabolism.
de Aguiar Vallim TQ, Tarling EJ, Ahn H, Hagey LR, Romanoski CE, Lee RG, Graham MJ, Motohashi H, Yamamoto M, Edwards PA., Free PMC Article | 03/26/2016 |
| 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. | Compound mouse mutants of bZIP transcription factors Mafg and Mafk reveal a regulatory network of non-crystallin genes associated with cataract.
Agrawal SA, Anand D, Siddam AD, Kakrana A, Dash S, Scheiblin DA, Dang CA, Terrell AM, Waters SM, Singh A, Motohashi H, Yamamoto M, Lachke SA., Free PMC Article | 08/22/2015 |
| These findings demonstrate that a combination of p45NF-E2, Maf G, and Maf K is a key determinant of both megakaryopoiesis and thrombopoiesis. | Induction of functional platelets from mouse and human fibroblasts by p45NF-E2/Maf.
Ono Y, Wang Y, Suzuki H, Okamoto S, Ikeda Y, Murata M, Poncz M, Matsubara Y., Free PMC Article | 01/5/2013 |
| 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. | Embryonic lethality and fetal liver apoptosis in mice lacking all three small Maf proteins.
Yamazaki H, Katsuoka F, Motohashi H, Engel JD, Yamamoto M., Free PMC Article | 03/31/2012 |
| The MafG C terminus is essential for proplatelet formation and platelet gene activation but not for p45 binding to the Maf recognition element (MARE). | Molecular determinants for small Maf protein control of platelet production.
Motohashi H, Fujita R, Takayama M, Inoue A, Katsuoka F, Bresnick EH, Yamamoto M., Free PMC Article | 01/29/2011 |
| mafG expression has intrinsic and extrinsic effects on hematopoietic engraftment following bone marrow transplantation. | Intrinsic and extrinsic effects of mafG deficiency on hematopoietic recovery following bone marrow transplant.
Li XM, Hu Z, Zafar AB, Jorgensen ML, Bungert J, Slayton W. | 01/15/2011 |
| determined the crystal structure of the MafG-DNA complex; each MafG monomer consists of three helices in which the carboxyl-terminal long helix organizes one DNA-contacting element and one coiled-coil dimer formation element. | Structural basis of alternative DNA recognition by Maf transcription factors.
Kurokawa H, Motohashi H, Sueno S, Kimura M, Takagawa H, Kanno Y, Yamamoto M, Tanaka T., Free PMC Article | 01/21/2010 |
| repression by MafG is not achieved through simple passive repression by competing for the activator binding site but requires sumoylation, which then mediates transcriptional repression through recruitment of a repressor complex | MafG sumoylation is required for active transcriptional repression.
Motohashi H, Katsuoka F, Miyoshi C, Uchimura Y, Saitoh H, Francastel C, Engel JD, Yamamoto M., Free PMC Article | 01/21/2010 |
| NMR structure of the DNA-binding domain of MafG | Solution structure of the DNA-binding domain of MafG.
Kusunoki H, Motohashi H, Katsuoka F, Morohashi A, Yamamoto M, Tanaka T. | 01/21/2010 |
| Thus compound mafG::mafK mutants develop age- and maf gene dosage-dependent cell-autonomous neuronal deficiencies that lead to profound neurological defects. | Small Maf compound mutants display central nervous system neuronal degeneration, aberrant transcription, and Bach protein mislocalization coincident with myoclonus and abnormal startle response.
Katsuoka F, Motohashi H, Tamagawa Y, Kure S, Igarashi K, Engel JD, Yamamoto M., Free PMC Article | 01/21/2010 |
| mafG is itself an ARE-dependent gene that is regulated by an Nrf2/small Maf heterodimer; there may be an autoregulatory feedback pathway for mafG transcriptional regulation | Nrf2 transcriptionally activates the mafG gene through an antioxidant response element.
Katsuoka F, Motohashi H, Engel JD, Yamamoto M. | 01/21/2010 |
| mafG::mafK::mafF triple-mutant fibroblasts that completely lack small Mafs are highly susceptible to oxidative stress.(mafG) | Genetic evidence that small maf proteins are essential for the activation of antioxidant response element-dependent genes.
Katsuoka F, Motohashi H, Ishii T, Aburatani H, Engel JD, Yamamoto M., Free PMC Article | 01/21/2010 |