| KAT6A deficiency impairs cognitive functions through suppressing RSPO2/Wnt signaling in hippocampal CA3. | KAT6A deficiency impairs cognitive functions through suppressing RSPO2/Wnt signaling in hippocampal CA3.
Liu Y, Fan M, Yang J, Mihaljević L, Chen KH, Ye Y, Sun S, Qiu Z., Free PMC Article | 08/15/2024 |
| Lysine acetyltransferase 6A maintains CD4[+] T cell response via epigenetic reprogramming of glucose metabolism in autoimmunity. | Lysine acetyltransferase 6A maintains CD4(+) T cell response via epigenetic reprogramming of glucose metabolism in autoimmunity.
Fu JY, Huang SJ, Wang BL, Yin JH, Chen CY, Xu JB, Chen YL, Xu S, Dong T, Zhou HN, Ma XY, Pu YP, Li H, Yang XJ, Xie LS, Wang ZJ, Luo Q, Shao YX, Ye L, Zong ZR, Wei XD, Xiao WW, Niu ST, Liu YM, Xu HP, Yu CQ, Duan SZ, Zheng LY. | 03/11/2024 |
| MOZ is critical for the development of MOZ/MLL fusion-induced leukemia through regulation of Hoxa9/Meis1 expression. | MOZ is critical for the development of MOZ/MLL fusion-induced leukemia through regulation of Hoxa9/Meis1 expression.
Katsumoto T, Ogawara Y, Yamagata K, Aikawa Y, Goitsuka R, Nakamura T, Kitabayashi I., Free PMC Article | 10/8/2022 |
| Identification of a specific program by which the chromatin modifier MOZ regulates craniofacial development. | MOZ directs the distal-less homeobox gene expression program during craniofacial development.
Vanyai HK, Garnham A, May RE, McRae HM, Collin C, Wilcox S, Smyth GK, Thomas T, Voss AK. | 07/11/2020 |
| Loss of MOZ in adult mice leads to the rapid loss of hematopoietic stem cells as defined by transplantation. | MOZ (KAT6A) is essential for the maintenance of classically defined adult hematopoietic stem cells.
Sheikh BN, Yang Y, Schreuder J, Nilsson SK, Bilardi R, Carotta S, McRae HM, Metcalf D, Voss AK, Thomas T. | 09/30/2017 |
| Our work revealed that MOZ and BMI1 regulate HSCs in a synergistic manner by acting on distinct processes required to maintain HSCs. | MOZ and BMI1 act synergistically to maintain hematopoietic stem cells.
Sheikh BN, Metcalf D, Voss AK, Thomas T. | 06/10/2017 |
| BRPF2-MOZ complexes play an important role in the differentiation of embryonic stem cells via H3K14 acetylation. | The BRPF2/BRD1-MOZ complex is involved in retinoic acid-induced differentiation of embryonic stem cells.
Cho HI, Kim MS, Jang YK. | 05/20/2017 |
| the expression of MOZ-TIF2 fusion protein represses the transcription of p16INK4a and p19ARF and blocks senescence. | Expression of the MOZ-TIF2 oncoprotein in mice represses senescence.
Largeot A, Perez-Campo FM, Marinopoulou E, Lie-a-Ling M, Kouskoff V, Lacaud G., Free PMC Article | 08/6/2016 |
| Study establishes that MOZ is an upstream inhibitor of the INK4A-ARF pathway, and suggests that inhibiting MOZ may be one way to induce senescence in proliferative tumor cells. | MOZ (MYST3, KAT6A) inhibits senescence via the INK4A-ARF pathway.
Sheikh BN, Phipson B, El-Saafin F, Vanyai HK, Downer NL, Bird MJ, Kueh AJ, May RE, Smyth GK, Voss AK, Thomas T. | 03/5/2016 |
| these data suggest that the molecular pathogenesis of ventricular septal defectss in Moz germline mutant mice is due to loss of MOZ-dependant activation of mesodermal Tbx1 and Tbx5 expression. | Mesodermal expression of Moz is necessary for cardiac septum development.
Vanyai HK, Thomas T, Voss AK. | 09/12/2015 |
| MOZ regulates B-cell progenitors and, consequently, Moz haploinsufficiency dramatically retards MYC-induced lymphoma development | MOZ regulates B-cell progenitors and, consequently, Moz haploinsufficiency dramatically retards MYC-induced lymphoma development.
Sheikh BN, Lee SC, El-Saafin F, Vanyai HK, Hu Y, Pang SH, Grabow S, Strasser A, Nutt SL, Alexander WS, Smyth GK, Voss AK, Thomas T., Free PMC Article | 05/30/2015 |
| These results suggest a critical requirement for MOZ HAT activity to silence p16(INK4a) expression and to protect stem cells from early entrance into replicative senescence. | MOZ-mediated repression of p16(INK) (4) (a) is critical for the self-renewal of neural and hematopoietic stem cells.
Perez-Campo FM, Costa G, Lie-A-Ling M, Stifani S, Kouskoff V, Lacaud G., Free PMC Article | 01/10/2015 |
| MOZ regulates B-cell memory formation, controlling memory compartment composition, an activity that is B cell-intrinsic and required for establishing the germinal center gene expression program. | Regulation of germinal center responses and B-cell memory by the chromatin modifier MOZ.
Good-Jacobson KL, Chen Y, Voss AK, Smyth GK, Thomas T, Tarlinton D., Free PMC Article | 09/27/2014 |
| MOZ interacts with the gene Tbx1 which influences heart and aortic arch development and is involved in DiGeorge syndrome. | Genetic modifier to chromatin may contribute to 22q11 deletion/VCF/DiGeorge syndrome variability: MOZ gene may also exacerbate effects of retinoic acid in genetic disorder.
Levenson D. | 08/10/2013 |
| The show that lack of the histone acetyltransferase MOZ (MYST3/KAT6A) phenocopies DiGeorge syndrome, and the MOZ complex occupies the Tbx1 locus, promoting its expression and histone 3 lysine 9 acetylation. | MOZ regulates the Tbx1 locus, and Moz mutation partially phenocopies DiGeorge syndrome.
Voss AK, Vanyai HK, Collin C, Dixon MP, McLennan TJ, Sheikh BN, Scambler P, Thomas T., Free PMC Article | 01/12/2013 |
| data show that Moz regulates H3K9 acetylation at Hox gene loci and that retinoic acid can act independently of Moz to establish specific Hox gene expression boundaries. | Moz and retinoic acid coordinately regulate H3K9 acetylation, Hox gene expression, and segment identity.
Voss AK, Collin C, Dixon MP, Thomas T. | 01/21/2010 |
| A specific role of MOZ-driven acetylation in controlling a desirable balance between proliferation and differentiation during hematopoiesis. | The histone acetyl transferase activity of monocytic leukemia zinc finger is critical for the proliferation of hematopoietic precursors.
Perez-Campo FM, Borrow J, Kouskoff V, Lacaud G., Free PMC Article | 01/21/2010 |
| Monocytic leukemia zinc finger (MOZ) interacts with p53 to induce p21 expression and cell-cycle arrest. | Monocytic leukemia zinc finger (MOZ) interacts with p53 to induce p21 expression and cell-cycle arrest.
Rokudai S, Aikawa Y, Tagata Y, Tsuchida N, Taya Y, Kitabayashi I. | 01/21/2010 |
| Moz is essential for a fundamental property of hematopoietic stem cells, the ability to reconstitute the hematopoietic system of a recipient after transplantation and that Moz is specifically required in the stem cell compartment. | Monocytic leukemia zinc finger protein is essential for the development of long-term reconstituting hematopoietic stem cells.
Thomas T, Corcoran LM, Gugasyan R, Dixon MP, Brodnicki T, Nutt SL, Metcalf D, Voss AK., Free PMC Article | 01/21/2010 |
| MOZ is required for maintenance of hematopoietic stem cells, and that it plays a role in differentiation of erythroid and myeloid cells. | MOZ is essential for maintenance of hematopoietic stem cells.
Katsumoto T, Aikawa Y, Iwama A, Ueda S, Ichikawa H, Ochiya T, Kitabayashi I., Free PMC Article | 01/21/2010 |