Zobrazeno 1 - 10
of 116
pro vyhledávání: '"Ash1l"'
Autor:
Gerry A. Shipman, Reinnier Padilla, Cynthia Horth, Bo Hu, Eric Bareke, Francisca N. Vitorino, Joanna M. Gongora, Benjamin A. Garcia, Chao Lu, Jacek Majewski
Publikováno v:
Genome Biology, Vol 25, Iss 1, Pp 1-28 (2024)
Abstract Background Methylation of histone 3 lysine 36 (H3K36me) has emerged as an essential epigenetic component for the faithful regulation of gene expression. Despite its importance in development and disease, how the molecular agents collectively
Externí odkaz:
https://doaj.org/article/452dd2d77ae044f69ef58363298ad192
Akademický článek
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Akademický článek
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Autor:
Al-Harthi, Samah
The human Absent, small, or homeotic disc1 (ASH1L) is a member of the Trithorax group (TrxG) proteins that play a role in epigenetic gene activation of developmental HOX genes via H3K36me2 methylation mark. ASH1L contains the evolutionarily conserved
Externí odkaz:
http://hdl.handle.net/10754/691382
Publikováno v:
Epigenetics & Chromatin, Vol 15, Iss 1, Pp 1-20 (2022)
Abstract The methylation of histone H3 at lysine 36 (H3K36me) is essential for maintaining genomic stability. Indeed, this methylation mark is essential for proper transcription, recombination, and DNA damage response. Loss- and gain-of-function muta
Externí odkaz:
https://doaj.org/article/1a37bd7da96549a9b3ff57e883da97f1
Autor:
Miaomiao Yu, Yanjie Jia, Zhanchuan Ma, Donglei Ji, Chunyu Wang, Yingying Liang, Qiang Zhang, Huanfa Yi, Lei Zeng
Publikováno v:
Frontiers in Oncology, Vol 12 (2022)
ASH1L is a member of the Trithorax-group protein and acts as a histone methyltransferase for gene transcription activation. It is known that ASH1L modulates H3K4me3 and H3K36me2/3 at its gene targets, but its specific mechanism of histone recognition
Externí odkaz:
https://doaj.org/article/8c2762d172c642199770859eb8aae394
Publikováno v:
Frontiers in Behavioral Neuroscience, Vol 16 (2022)
ASH1L is one of the highest risk genes associated with autism spectrum disorder (ASD) and intellectual disability (ID). Our recent studies demonstrate that loss of Ash1l in the mouse brain is sufficient to induce ASD/ID-like behavioral and cognitive
Externí odkaz:
https://doaj.org/article/ca98b6619f28456aa7c316be8332d25a
Autor:
Wenmiao Liu, Lulu Xu, Cheng Zhang, Lu Shen, Jicheng Dong, Han Zhang, Shiguo Liu, Fengyuan Che, Xueping Zheng
Publikováno v:
Brain and Behavior, Vol 12, Iss 4, Pp n/a-n/a (2022)
Abstract Objective Tourette syndrome (TS) is a childhood neurodevelopmental disorder caused by various genetic and environmental factors and presents with apparent genetic heterogeneity. As ASH1L potentially contributes to neurodevelopmental diseases
Externí odkaz:
https://doaj.org/article/edb2fb51dd364eb9933b56112321cfe8
Publikováno v:
Molecular Cytogenetics, Vol 13, Iss 1, Pp 1-6 (2020)
Abstract Background Copy number variants (CNVs) associated with developmental delay and intellectual disability (DD/ID) continue to be identified in patients. This article reports identification of a chromosome 1q22 microdeletion as the genetic cause
Externí odkaz:
https://doaj.org/article/56ae58fa118c40e2af945138797f552d