Results 61 to 70 of about 604,881 (306)

MITF maintains genome stability in nonmelanocyte lineages

Molecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir, Adrián López García de Lomana, Thejus B. Venkatesh, Kritika Kirty, Snaevar Sigurdsson, Linda Vidarsdottir, Ramile Dilshat, Erla Sveinbjornsdottir, Snaedis Ragnarsdottir, Daniel H Magnusson, Maria R. Bustos, Eirikur Steingrimsson, Thorkell Gudjonsson, Stefan Sigurdsson   +13 more
wiley   +1 more source

ChIP-Seq and RNA-Seq datasets with corresponding ID.

, 2019
ChIP-Seq and RNA-Seq datasets with corresponding ID.
Aiindrila Dhara (7512545), Nirmalya Sen (7512548), Pritish Kumar Varadwaj (7512551), Imlimaong Aier (691334), Rahul Semwal (7512542)   +4 more
core   +1 more source

Quantifying the impact of inter-site heterogeneity on the distribution of ChIP-seq data

Frontiers in Genetics, 2014
Chromatin Immunoprecipitation followed by sequencing (ChIP-seq) is a valuable tool for epigenetic studies. Analysis of the data arising from ChIP-seq experiments often requires implicit or explicit statistical modelling of the read counts.
Jonathan eCairns, Jonathan eCairns, Andy G Lynch, Simon eTavaré   +3 more
doaj   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

Molecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu, Nicolas J. Niklaus, Anna M. Schläfli, Igor Tokarchuk, Magali Humbert, Federico La Manna, Bich Vu, David Maul, Ramin Radpour, Marianna Kruithof‐de Julio, Inti Zlobec, Jörn Dengjel, Bruce E. Torbett, Mario P. Tschan   +13 more
wiley   +1 more source

Epigenetic silencing of the liver‐specific lncRNA LUNAR promotes liver cancer progression via NOTCH activation

Molecular Oncology, EarlyView.
LUNAR is a liver‐specific long noncoding RNA (lncRNA) that is highly expressed in normal liver but becomes epigenetically silenced in hepatocellular carcinoma through promoter hypermethylation. Loss of LUNAR is associated with NOTCH activation, epithelial–mesenchymal transition, and metastasis, whereas restoring LUNAR restrains metastatic progression ...
Se Ha Jang, Hyung Seok Kim, Geum Ok Baek, Moon Gyeong Yoon, Su In Lee, Jee‐Yeong Jeong, Ji Eun Han, Soon Sun Kim, Jae Youn Cheong, Jung Woo Eun   +9 more
wiley   +1 more source

xcore: an R package for inference of gene expression regulators

BMC Bioinformatics, 2023
Background Elucidating the Transcription Factors (TFs) that drive the gene expression changes in a given experiment is a common question asked by researchers.
Maciej Migdał, Takahiro Arakawa, Satoshi Takizawa, Masaaki Furuno, Harukazu Suzuki, Erik Arner, Cecilia Lanny Winata, Bogumił Kaczkowski   +7 more
doaj   +1 more source

CEACAM1 participation in breast cancer progression

Molecular Oncology, EarlyView.
In invasive breast cancer (BC), CEACAM1 shifts from an apical to a uniform membranous/cytoplasmic pattern, or is lost, as tumors dedifferentiate, inversely tracking the Ki‐67 proliferative index. In MCF‐7 cells, only CEACAM1‐4L suppresses proliferation, repressing cell cycle and growth factor genes.
Mykola Lyndin, Irina Kube‐Golovin, Anatolii Romaniuk, Gunther Wennemuth   +3 more
wiley   +1 more source

An optimized protocol for rapid, sensitive and robust on-bead ChIP-seq from primary cells

STAR Protocols, 2021
Summary: Integrative analysis of next-generation sequencing data can help understand disease mechanisms. Specifically, ChIP-seq can illuminate where transcription regulators bind to regulate transcription.
Lorane Texari, Nathanael J. Spann, Ty D. Troutman, Mashito Sakai, Jason S. Seidman, Sven Heinz   +5 more
doaj   +1 more source

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

Molecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico, Veronica La Banca, Silvia D'Amico, Stefano Scalera, Sara Nicolai, Angelo Peschiaroli   +5 more
wiley   +1 more source

An integrated pipeline for the genome-wide analysis of transcription factor binding sites from ChIP-Seq.

PLoS ONE, 2011
ChIP-Seq has become the standard method for genome-wide profiling DNA association of transcription factors. To simplify analyzing and interpreting ChIP-Seq data, which typically involves using multiple applications, we describe an integrated, open source,
Eloi Mercier, Arnaud Droit, Leping Li, Gordon Robertson, Xuekui Zhang, Raphael Gottardo   +5 more
doaj   +1 more source