日期:
2020 年 — 2026 年
2020
2021
2022
2023
2024
2025
2026
影响因子:

The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer.

组蛋白甲基转移酶 KMT2D 是去势抵抗性前列腺癌谱系可塑性和治疗反应的关键介质。

Kittane Srushti, Ladewig Erik, Li Taibo, Love Jillian R, Blawski Ryan, Gao Yangzhenyu, Arruabarrena-Aristorena Amaia, Zhao Peihua, Dalrymple Susan L, Liu Huayang, Guo Xinyu, Sallaku Mirna, Kelkar Nachiket, Garcia-Martinez Liliana, Carmona Sanz Javier, Chen Wanlu, Stoudmann Candice, Baldino Laura, Razavi-Mohseni Milad, Kalemi Ingrid, Beer Michael A, Castel Pau, Brennen W Nathaniel, Scaltriti Maurizio, Morey Lluis, Cocco Emiliano, Ji Hongkai, Chan Ho Man, Battle Alexis, Leslie Christina S, Karthaus Wouter R, Toska Eneda

Expanding the Anatomical Distribution of PRRX1::KMT2D Fusion Mesenchymal Neoplasms: A Rare Mediastinal Case Report

PRRX1::KMT2D融合间叶肿瘤的解剖分布范围扩大:一例罕见的纵隔病例报告

Zhong, Weixiang; Deng, Yu; Sun, Ke

Histone methylation activity of KMT2D is required for proliferative control of the developing lung

KMT2D的组蛋白甲基化活性对于发育中肺的增殖控制是必需的。

Mehta, Aalekh S; Xie, Guojia; High, Frances A; Donahoe, Patricia K; Rowbotham, Samuel P

Chromatin modifiers KMT2D, BAF, and p300 are required for de novo binding of transcription factors on enhancers.

染色质修饰因子 KMT2D、BAF 和 p300 是转录因子在增强子上从头结合所必需的。

Van Hieu T, Park Young-Kwon, Liu Chengyu, Islam Shamima, Dell'Orso Stefania, Peng Weiqun, Sartorelli Vittorio, Lee Ji-Eun, Ge Kai

KMT2C and KMT2D amplify GRHL2-driven enhancer activation.

KMT2C 和 KMT2D 可增强 GRHL2 驱动的增强子激活。

Boileau Ryan M, Chen Kevin X, Blelloch Robert

KMT2D temporally activates neuronal transcriptional factor genes to mediate cerebellar granule cell differentiation

KMT2D 可暂时激活神经元转录因子基因,从而介导小脑颗粒细胞分化。

Dhar, Shilpa S; Ko, Kyung-Pil; Jang, Jinho; Brown-Abel, Calena; Lin, Tao; Awasthi, Sharad; Chen, Kaifu; Sillitoe, Roy V; Park, Jae-Il; Lee, Min Gyu

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

组蛋白甲基转移酶 KMT2D 靶向 SPOP-G3BP1 轴,以增强 AR 稳定性并驱动去势抵抗性前列腺癌的进展。

Wen Haoran, Maheremu Maierhaba, Zhang Kaidi, Bao Liuru, Luo Mayao, Zhang Yifan, Liao Yuanpeng, Zhou Manli, Wu Chenwei, Lv Shidong, Qiu Xiaofu, Wei Qiang

KMT2D coordinates antiviral CD4+ T cell responses through opposing effects on T follicular helper and cytotoxic gene expression

KMT2D通过对滤泡辅助性T细胞和细胞毒性基因表达的相反作用来协调抗病毒CD4+ T细胞反应。

Jonathan A Cohen ,Ashlyn A Buzzelli ,Gabrielle Quickstad ,Lixin Yang ,Ichiro Misumi ,Karl B Shpargel ,Jason K Whitmire

KMT2C/KMT2D-dependent H3K4me1 mediates changes in DNA replication timing and origin activity during a cell fate transition

KMT2C/KMT2D依赖的H3K4me1介导细胞命运转变过程中DNA复制时间和复制起始位点活性的变化

Deniz Gökbuget ,Liana Goehring ,Ryan M Boileau ,Kayla Lenshoek ,Tony T Huang ,Robert Blelloch

In vivo CRISPR screening reveals cooperation of KMT2D and TP53 deficiencies in B-cell lymphomagenesis

体内 CRISPR 筛选揭示 KMT2D 和 TP53 缺陷在 B 细胞淋巴瘤发生中的协同作用

Yamaguchi, Kentaro; Koya, Junji; Mizuno, Kota; Mizukami, Yosuke; Yoshifuji, Kota; Saito, Yuki; Tabata, Mariko; Shingaki, Sumito; Yuasa, Mitsuhiro; Ito, Yuta; Nakashima, Kazutaka; Dreval, Kostiantyn; Morin, Ryan D; Chiba, Kenichi; Okada, Ai; Shiraishi, Yuichi; Murakami, Koichi; Kogure, Yasunori; Ohshima, Koichi; Kataoka, Keisuke