Results 1 to 10 of about 13,098 (199)

Contrasting roles of KMT2C and KMT2D in breast cancer [PDF]

open access: yesScientific Reports
KMT2C and KMT2D are paralogous lysine-methyltransferases that primarily monomethylate lysine residues at enhancer regions promoting an active transcriptional state.
Emily Tinsley   +4 more
doaj   +7 more sources

Deficiency of KMT2D causes autistic-like behavior in mice and zebrafish [PDF]

open access: yesCommunications Biology
Kabuki syndrome type 1 is a congenital multisystem disorder caused by KMT2D mutations. While some studies suggest that KMT2D deficiency may lead to autistic-like behaviors, the role of KMT2D in social behavior remains unconfirmed due to a lack of animal ...
Huakun Shangguan   +11 more
doaj   +6 more sources

Role of histone methyltransferase KMT2D in BMSC osteogenesis via AKT signaling

open access: yesRegenerative Therapy
Understanding the precise mechanism of BMSC (bone marrow mesenchymal stem cell) osteogenesis is critical for metabolic bone diseases and bone reconstruction. The histone-lysine N-methyltransferase 2D (KMT2D) acts as an important methyltransferase related
Xuejun Gao
exaly   +6 more sources

Role of histone-lysine N-methyltransferase 2D (KMT2D) in MEK-ERK signaling-mediated epigenetic regulation: a phosphoproteomics perspective [PDF]

open access: yesFrontiers in Bioinformatics
IntroductionHistone-lysine N-methyltransferase 2D (KMT2D) is an H3K4 methyltransferase and a potential tumor suppressor with a crucial role in regulating gene expression.
Sreeshma Ravindran Kammarambath   +9 more
doaj   +3 more sources

Heterozygous Kmt2d loss diminishes enhancers to render medulloblastoma cells vulnerable to combinatory inhibition of LSD1 and OXPHOS

open access: yesCell Reports
Summary: The histone H3 lysine 4 (H3K4) methyltransferase KMT2D (also called MLL4) is one of the most frequently mutated epigenetic modifiers in many cancers, including medulloblastoma (MB).
Shilpa Dhar, Min Gyu Lee
exaly   +4 more sources

KMT2D Deficiency Promotes Myeloid Leukemias which Is Vulnerable to Ribosome Biogenesis Inhibition

open access: yesAdvanced Science, 2023
KMT2C and KMT2D are the most frequently mutated epigenetic genes in human cancers. While KMT2C is identified as a tumor suppressor in acute myeloid leukemia (AML), the role of KMT2D remains unclear in this disease, though its loss promotes B cell ...
Yu Liu
exaly   +3 more sources

Histone methyltransferase KMT2D targets the SPOP-G3BP1 axis to enhance AR stability and drive castration-resistant prostate cancer progression [PDF]

open access: yesMol Biomed
Castration-resistant prostate cancer (CRPC) poses a significant clinical challenge, characterized by limited therapeutic options and unfavorable prognosis, particularly among elderly men.
Haoran Wen   +11 more
semanticscholar   +2 more sources

Histone-methyltransferase KMT2D deficiency impairs the Fanconi anemia/BRCA pathway upon glycolytic inhibition in squamous cell carcinoma

open access: yesNature Communications
Histone lysine methyltransferase 2D (KMT2D) is the most frequently mutated epigenetic modifier in head and neck squamous cell carcinoma (HNSCC).
Wei Liu   +10 more
doaj   +2 more sources

Preliminary investigation of the epigenetic regulation of KMT2D via H3K4me1/H3K27ac in oral squamous cell carcinoma

open access: yesCellular and Molecular Life Sciences
Histone lysine methyltransferase 2D (KMT2D/MLL4) critically modulates gene expression by methylating and acetylating histones H3K4/H3K27, thereby regulating the expression of specific target genes. Although KMT2D is highly mutated in a variety of cancers,
Mujie Yuan   +9 more
doaj   +2 more sources

Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma

open access: yesCell Reports, 2020
Summary: Histone methyltransferase KMT2D harbors frequent loss-of-function somatic point mutations in several tumor types, including melanoma. Here, we identify KMT2D as a potent tumor suppressor in melanoma through an in vivo epigenome-focused pooled ...
Yu-Hsi Lin   +2 more
exaly   +3 more sources

Home - About - Disclaimer - Privacy