Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mass spectrometry-based validation of BPTF knockout in human induced pluripotent stem cells

ABSTRACT: We generated a BPTF knockout human induced pluripotent stem cell (iPSC) line using CRISPR-Cas9 and confirmed loss of the targeted locus by genotyping. Quantitative mass spectrometry verified complete absence of BPTF protein in the knockout clone. This validated line was used for downstream functional assays in the somitoid system, a 3D iPSC-derived model that recapitulates early human somite development.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Stem Cell, Hipsc Cell

SUBMITTER: S Stelloo

LAB HEAD: Michiel vermeulen

PROVIDER: PXD068407 | Pride | 2026-08-07

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20250910_Astral2_AUR_MA_30SPD_WCE_SP3_hiPSCs_BPTF_KO_1.raw	Raw
	20250910_Astral2_AUR_MA_30SPD_WCE_SP3_hiPSCs_BPTF_KO_2.raw	Raw
	20250910_Astral2_AUR_MA_30SPD_WCE_SP3_hiPSCs_BPTF_KO_3.raw	Raw
	20250910_Astral2_AUR_MA_30SPD_WCE_SP3_hiPSCs_WT_1.raw	Raw
	20250910_Astral2_AUR_MA_30SPD_WCE_SP3_hiPSCs_WT_2.raw	Raw

Items per page:

1 - 5 of 8

Similar Datasets

BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [RNA-Seq]

Project description:The c-MYC oncogene is a key transcription factor deregulated in most human tumors. Histone marks associated with transcriptionally active genes in euchromatic islands define the set of high-affinity c-MYC targets. The mechanisms involved in their recognition by c-MYC are not known but likely involve chromatin-remodelling and chromatin-modifying complexes. Here, we show that c-MYC interacts with BPTF, a core subunit of the NURF complex that binds active chromatin. BPTF is required for the activation of the full c-MYC transcriptional programme in fibroblasts. BPTF knockdown leads to a decrease in c-MYC recruitment to DNA and to changes in chromatin accessibility. Using BPTF-null MEFs we show that BPTF is necessary for c-MYC-driven proliferation, G1-S progression, and replication stress, but not for c-MYC-driven apoptosis. Consistently, BPTF is required for the proliferation of cells driven by c-MYC, such as Burkitt lymphoma, and its expression in human cancer lines correlates with the activation of c-MYC gene signatures. Our findings point to the c-MYC-BPTF axis as a potential therapeutic target in cancer. To assess whether BPTF is required for the transcriptional activity of c-MYC, human foreskin fibroblasts (HFF) were stably transduced with the chimeric MYC-ER cDNA (HFF MYC-ER) and infected with lentiviruses coding for either control (shNt) or BPTF-targeting shRNAs. Cells were serum-starved for 2 days to achieve quiescence and then treated with 4-hydroxytamoxifen (4-OHT)

2016-01-19 | E-GEOD-65545 | biostudies-arrayexpress

BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [ChIP-Seq]

2016-01-19 | E-GEOD-65544 | biostudies-arrayexpress

Transcriptomic analysis of Bptf wild-type and Bptf heterozygous lymphomas arising from Em-Myc tumors

Project description:Purpose: Evaluation of the impact of a reduction in Bptf levels on the nature of lymphomas arising from Em-Myc mice. Results: Bptf heterozygous tumors show reduced activity of the E2F and c-MYC pathways, together with increased activity of the NF-kB pathway.

2019-12-10 | GSE141647 | GEO

BPTF Depletion Enhances NK Cell Mediated Antitumor Immunity

Project description:In mouse models, the bromodomain PHD finger transcription factor (BPTF) chromatin remodeling subunit in tumor cells suppresses natural killer (NK) cell antitumor activity. In vitro, BPTF suppresses NK cell cytolytic activity to mouse and human cancer cell lines, demonstrating a conserved function.

2017-04-28 | GSE85756 | GEO

BPTF regulstes androgen receptor activity by enhancing chromatin accessibility and stabilizing the AR-FOXA1 interaction

Project description:BPTF, the scaffolding subunit of the nucleosome remodeling factor (NURF) complex, has been implicated in the progression of various malignancies. However, its role in prostate cancer (PCa) remains poorly understood. Here, we demonstrate that BPTF is upregulated in castration-resistant prostate cancer (CRPC) and promotes disease progression. RNA-seq revealed that BPTF primarily upregulates the expression of androgen receptor (AR) target genes. ChIP-seq showed that BPTF facilitates AR binding to enhancers and super-enhancers, while ATAC-seq demonstrated that BPTF increases chromatin accessibility to facilitate AR binding, partly via SMARCA1, a catalytic subunit of the NURF complex. Notably, BPTF/AR shared ChIP-seq peaks are highly enriched for FOXA1 motifs but only weakly enriched for AR motifs. We find that BPTF interacts with both FOXA1 and AR to form a protein complex in which FOXA1 recruits BPTF-AR to chromatin, while BPTF stabilizes the AR–FOXA1 interaction. Importantly, BPTF interacts with AR through its bromodomain, and a BPTF bromodomain inhibitor disrupts this interaction, leading to impaired AR signaling and suppressed PCa cell growth. In summary, our findings establish BPTF as a critical regulator of AR activity by promoting chromatin accessibility and stabilizing the AR–FOXA1 complex, highlighting BPTF as a potential therapeutic target in prostate cancer.

2025-11-13 | GSE287918 | GEO

BPTF regulstes androgen receptor activity by enhancing chromatin accessibility and stabilizing the AR-FOXA1 interaction [RNA-Seq]

2025-11-17 | GSE287905 | GEO

BPTF regulstes androgen receptor activity by enhancing chromatin accessibility and stabilizing the AR-FOXA1 interaction [Cut&Run]

2025-11-17 | GSE287902 | GEO

BPTF regulstes androgen receptor activity by enhancing chromatin accessibility and stabilizing the AR-FOXA1 interaction [ATAC-Seq]

2025-11-17 | GSE287901 | GEO

BPTF is essential for murine neocortical development

Project description:Chromatin remodeling complexes modulate DNA accessibility permitting neuronal progenitor cells to proliferate and differentiate to form the mammalian neocortex. In the case of BPTF, the major subunit of a chromatin remodelling complex called NURF, mutations leading to its haploinsufficiency have been linked to cause a recently annotated human neurodevelopmental disorder called NEDDFL (Neurodevelopmental disorder with dysmorphic facies and distal limb anomalies). Patients with this syndrome are mainly characterized with microcephaly and intellectual disability. We conditionally knockout (cKO) the Bptf gene during neocortical neurogenesis to analyze its role during embryonic and postnatal brain development. The Bptf cKO animals reveal significant forebrain hypoplasia. During cortical neurogenesis, the cKOs show a reduction in intermediate neuronal progenitor (INP) cells, an increase in apoptosis as well as a prolonged cell cycle of proliferating progenitors. Similarly, the cKOs have decreased proportions of pyramidal neurons expressing Ctip2 and Foxp1. Lastly, our RNA-seq analysis delineates gene pathways deregulated by Bptf’s removal, which are involved in neurogenesis and neuronal differentiation. Our results indicate that Bptf is critical for murine telencephalon neurogenesis. The hypoplasia demonstrated in the mouse model can resemble the microcephaly displayed by the human NEDFFL patients, highlighting the relevance of chromatin remodelling complexes during intricate neural developmental processes.

2022-03-31 | GSE154700 | GEO

BPTF inhibitor increases gastric cancer response to Erlotinib by epigenetically regulating c-MYC/PLCG1/pErk axis [RNA-seq]

Project description:To understand how BPTF conferred resistance to Erlotinib in GC cells, we performed transcriptome profiling (RNA-seq) in MGC803/BPTF-KO and MGC803/BPTF-NC cells.

2023-12-13 | GSE200182 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data