Functional role of Ash2l in oxLDL induced endothelial dysfunction and atherosclerosis. | Functional role of Ash2l in oxLDL induced endothelial dysfunction and atherosclerosis. Su Z, Wang J, Xiao C, Zhong W, Liu J, Liu X, Zhu YZ., Free PMC Article | 02/4/2024 |
ASH2L-mediated H3K4me3 drives diabetic nephropathy through HIPK2 and Notch1 pathway. | ASH2L-mediated H3K4me3 drives diabetic nephropathy through HIPK2 and Notch1 pathway. Zhong W, Hong C, Zhang Y, Li Y, Xiao C, Liu X. | 01/16/2024 |
ASH2L, Core Subunit of H3K4 Methylation Complex, Regulates Amelogenesis. | ASH2L, Core Subunit of H3K4 Methylation Complex, Regulates Amelogenesis. Zhu X, Ma Z, Xie F, Wang J. | 01/3/2024 |
ASH2L regulates postnatal neurogenesis through Onecut2-mediated inhibition of TGF-beta signaling pathway. | ASH2L regulates postnatal neurogenesis through Onecut2-mediated inhibition of TGF-β signaling pathway. Xu YJ, Dai SK, Duan CH, Zhang ZH, Liu PP, Liu C, Du HZ, Lu XK, Hu S, Li L, Teng ZQ, Liu CM., | 08/10/2023 |
ASH2L Controls Ureteric Bud Morphogenesis through the Regulation of RET/GFRA1 Signaling Activity in a Mouse Model. | ASH2L Controls Ureteric Bud Morphogenesis through the Regulation of RET/GFRA1 Signaling Activity in a Mouse Model. Zhao Z, Dai X, Jiang G, Lin F., | 06/13/2023 |
Loss of the Ash2l subunit of histone H3K4 methyltransferase complexes reduces chromatin accessibility at promoters. | Loss of the Ash2l subunit of histone H3K4 methyltransferase complexes reduces chromatin accessibility at promoters. Barsoum M, Stenzel AT, Bochyńska A, Kuo CC, Tsompanidis A, Sayadi-Boroujeni R, Bussmann P, Lüscher-Firzlaff J, Costa IG, Lüscher B., Free PMC Article | 03/3/2023 |
ASH2L Aggravates Fibrosis and Inflammation through HIPK2 in High Glucose-Induced Glomerular Mesangial Cells. | ASH2L Aggravates Fibrosis and Inflammation through HIPK2 in High Glucose-Induced Glomerular Mesangial Cells. Zhong W, Hong C, Dong Y, Li Y, Xiao C, Liu X., Free PMC Article | 01/11/2023 |
The Ash2l SDI Domain Is Required to Maintain the Stability and Binding of DPY30. | The Ash2l SDI Domain Is Required to Maintain the Stability and Binding of DPY30. Ma M, Zhou J, Ma Z, Chen H, Li L, Hou L, Yin B, Qiang B, Shu P, Peng X., Free PMC Article | 05/21/2022 |
Hematopoietic stem and progenitor cell proliferation and differentiation requires the trithorax protein Ash2l. | Hematopoietic stem and progenitor cell proliferation and differentiation requires the trithorax protein Ash2l. Lüscher-Firzlaff J, Chatain N, Kuo CC, Braunschweig T, Bochyńska A, Ullius A, Denecke B, Costa IG, Koschmieder S, Lüscher B., Free PMC Article | 10/31/2020 |
The COMPASS Family Protein ASH2L Mediates Corticogenesis via Transcriptional Regulation of Wnt Signaling. | The COMPASS Family Protein ASH2L Mediates Corticogenesis via Transcriptional Regulation of Wnt Signaling. Li L, Ruan X, Wen C, Chen P, Liu W, Zhu L, Xiang P, Zhang X, Wei Q, Hou L, Yin B, Yuan J, Qiang B, Shu P, Peng X. | 08/29/2020 |
Transfection of Ash2l with W118A mutation to disrupt Ash2l-Oct4 interaction fails to rescue Ash2l-driven enhancer activation and pluripotent gene upregulation in Ash2l-depleted pluripotent stem cells. Together, our data demonstrated Ash2l formed an enhancer-bound Ash2l/OSN complex that can drive enhancer activation, govern pluripotency network and stemness circuitry. | Ash2l interacts with Oct4-stemness circuitry to promote super-enhancer-driven pluripotency network. Tsai PH, Chien Y, Wang ML, Hsu CH, Laurent B, Chou SJ, Chang WC, Chien CS, Li HY, Lee HC, Huo TI, Hung JH, Chen CH, Chiou SH., Free PMC Article | 12/14/2019 |
OCT4 directly activates expression of Ash2l-b. | Disruption of OCT4 Ubiquitination Increases OCT4 Protein Stability and ASH2L-B-Mediated H3K4 Methylation Promoting Pluripotency Acquisition. Li S, Xiao F, Zhang J, Sun X, Wang H, Zeng Y, Hu J, Tang F, Gu J, Zhao Y, Jin Y, Liao B., Free PMC Article | 09/21/2019 |
Ash2l-1 and Ash2l-2 are involved in the maintenance of mESCs pluripotency and the regulation of genomic H3K4me3. | Expression specificity and compensation effect of Ash2l-1/Ash2l-2 in mouse embryonic stem cells. Xie J, Fan C, Zhang JL, Zhang SQ. | 07/7/2018 |
We discuss the implications of these results to understand the role of ASH2L and Xist repeat E for histone modifications and escape gene regulation during random X-chromosome inactivation. | Xist RNA repeat E is essential for ASH2L recruitment to the inactive X and regulates histone modifications and escape gene expression. Yue M, Ogawa A, Yamada N, Charles Richard JL, Barski A, Ogawa Y., Free PMC Article | 08/5/2017 |
ASH2L enhances ERalpha expression as a coactivator of GATA3 in breast cancers | Absent, small or homeotic 2-like protein (ASH2L) enhances the transcription of the estrogen receptor α gene through GATA-binding protein 3 (GATA3). Qi J, Huo L, Zhu YT, Zhu YJ., Free PMC Article | 01/24/2015 |
Ash2l is essential for pluripotency and maintaining open chromatin in embryonic stem cells | The trithorax group protein Ash2l is essential for pluripotency and maintaining open chromatin in embryonic stem cells. Wan M, Liang J, Xiong Y, Shi F, Zhang Y, Lu W, He Q, Yang D, Chen R, Liu D, Barton M, Songyang Z., Free PMC Article | 05/4/2013 |
Tbx1 and Ash2l have overlapping mRNA and protein expression patterns during development. | Ash2l interacts with Tbx1 and is required during early embryogenesis. Stoller JZ, Huang L, Tan CC, Huang F, Zhou DD, Yang J, Gelb BD, Epstein JA., Free PMC Article | 05/31/2010 |
Several candidate targets of complexes containing Ap2delta and Ash2l were identified that can be used to further elucidate their roles during development and showed that Fgfr3 is a novel direct target of these complexes. | Fgfr3 is a transcriptional target of Ap2delta and Ash2l-containing histone methyltransferase complexes. Tan CC, Walsh MJ, Gelb BD., Free PMC Article | 03/22/2010 |
Ap2delta associates with ASH2L and MLL2 (ALR), forming a complex that methylates lysine 4 of histone H3. | Transcription factor Ap2delta associates with Ash2l and ALR, a trithorax family histone methyltransferase, to activate Hoxc8 transcription. Tan CC, Sindhu KV, Li S, Nishio H, Stoller JZ, Oishi K, Puttreddy S, Lee TJ, Epstein JA, Walsh MJ, Gelb BD., Free PMC Article | 01/21/2010 |