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BLM-G4 pulldown IP-MS in human colon cancer HT-29 cells

ABSTRACT: the experiment uses biotin-labelled BLM-G4 to incubate with HT-29 cell lysates, and uses streptavidin agarose beads to pulldown BLM-G4-binding proteins. Utilize LC-MS/MS to annotate and quantify the proteins pulled down by BLM-G4.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Malignant Cell, Cell Culture

DISEASE(S): Colon Cancer

SUBMITTER: Yingying Wang

LAB HEAD: Kaibo Wang

PROVIDER: PXD075345 | Pride | 2026-06-08

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	BLM_G4_MUT_1.raw	Raw
	BLM_G4_MUT_2.raw	Raw
	BLM_G4_MUT_3.raw	Raw
	BLM_G4_WT_1.raw	Raw
	BLM_G4_WT_2.raw	Raw

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1 - 5 of 9

Publications

A small molecule disrupts G4-STAT1 interaction and synergizes with olaparib to drive cancer cell death.

Wang Yingying Y Zhang Xuenan X Bian Yuting Y He Sihan S Cheng Rongshuang R Li Jinzhu J Dickerhoff Jonathan J Liu Yushuang Y Zhou Yu Y Bian Jinlei J Zheng Kewei K Yang Danzhou D Kong Ling-Yi LY Wang Kai-Bo KB

Nucleic acids research 20260501 9

Bloom syndrome protein (BLM), a RecQ family DNA helicase, is consistently overexpressed in multiple malignancies, yet its therapeutic potential remains largely unexplored. Herein, we focused on targeting the BLM promoter G-quadruplex (BLM-G4) to inhibit the BLM signaling pathway. We first characterized the parallel BLM-G4 in the BLM promoter region. Subsequently, it is shown for the first time that BLM-G4 recruits phosphorylated signal transducer and activator of transcription 1 (pSTAT1) to acti ...[more]

PMID: 42087785

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Effect of TOPBEffect of TOPBP1 on BLM phosphosites

Project description:Identification of BLM phosphosites. The experiment is composed by 2 parts: i) identification of BLM phosphosites with DDA method ii) quantification of phosphosites with a targeted method.

2021-11-25 | PXD026460 | Pride

Proteome-wide Identification of DNA Guanine Quadruplex-binding Proteins

Project description:DNA sequences of high guanine (G) content have the potential to fold into G quadruplex (G4) structures. DNA G4 is known to play important roles in various cellular processes including DNA replication, transcriptional regulation, and maintenance of genomic integrity. A more complete understanding about the biological functions of G4 DNA requires the investigation about how these structures are recognized by cellular proteins. Here, we conducted exhaustive quantitative proteomic experiments to profile the interaction proteomes of three well-defined G4 structures derived from the human telomere and the promoters of cMYC and cKIT genes. Our results led to the identification of a number of candidate G4-interacting proteins; some were previously reported, e.g., FUS, TOP1, and PARP1, and many others were discovered here for the first time. These included three proteins that can bind to all three DNA G4 structures and many proteins that can bind specifically to selected DNA G4 structure(s). We also validated that GRSF1 can bind directly and selectively toward G4 DNA structure derived from the cMYC promoter. Taken together, we uncovered a number of cellular proteins that exhibit general and selective recognitions of G4 folding patterns, which underscore the complexity of G4 DNA in biology and the importance in understanding fully the G4-interaction proteome.

2021-09-29 | PXD026794 | Pride

Identification BLM phosphosites in presence or absence of lambda phosphatase

Project description:Identification of BLM phosphosites in presence or absence of lambda phosphatase. DDA analysis of purified protein

2021-11-25 | PXD026452 | Pride

DNA-damaging agent and immune inducer synergistically induced defence gene expression in Arabidopsis

Project description:We used microarrays to identify differentially expressed genes after DNA-damaging agent bleomycin (BLM) and/or immune inducer 2, 6-dichloroisonicotinic acid (INA) treatment. We focused on those genes that were synergistically induced by co-treatment (BLM+INA). Arabidopsis seedlings were treated with 4 μg/ml BLM and/or low INA (10 μM). There are 4 treatments: control (CK), INA, BLM and BLM+INA. Each treatments have three biological replicates. There are 12 samples in total.

2013-11-14 | E-GEOD-44793 | biostudies-arrayexpress

Small Molecule Disrupts G4-STAT1 Interaction and Synergizes with Olaparib to Drive Cancer Cell Death

Project description:Bloom syndrome protein (BLM), a RecQ family DNA helicase, is consistently overexpressed in multiple malignancies, yet its therapeutic potential remains largely unexplored. Herein, we focused on targeting the BLM promoter G-quadruplex (BLM-G4) to inhibit the BLM signaling pathway. We first characterized the parallel BLM-G4 in BLM promoter region. Subsequently, it is evidenced for the first time that BLM-G4 recruits phosphorylated STAT1 to activate BLM expression. Importantly, two natural alkaloids, berberine (BER) and coptisine (COP), compete with STAT1 for binding to BLM-G4, thereby significantly suppressing BLM expression in colon cancer cells. The BER/COP-BLM-G4 complex structures were determined using NMR experiments, which provide valuable insights for the rational design of next-generation BLM-G4-targeting ligands. Beyond BLM regulation, the conjoint analysis of genome-wide STAT1-CUT&Tag-seq, G4P-CUT&Tag-seq, and RNA-seq demonstrated STAT1 as a general G4-binding transcription factor and COP as a pan-genomic G4 stabilizer. Furthermore, BER/COP exhibited a pronounced synergistic effect with Olaparib in inducing colon cancer cell death by disrupting DNA repair pathways and intensifying DNA damage. Collectively, our findings reveal a novel epigenetic mechanism of BLM gene upregulation mediated by BLM-G4-STAT1 interaction and suggest that the combination therapy of G4 stabilizers with PARP inhibitors is a promising strategy for treating complex cancers.

2026-05-15 | GSE324248 | GEO

Centromere protection requires strict mitotic inactivation of the Bloom syndrome helicase complex

Project description:The BTRR (BLM/TOP3A/RMI1/RMI2) complex resolves various DNA replication and recombination intermediates to suppress genome instability. Alongside PICH, they target mitotic DNA intertwinements, known as ultrafine DNA bridges, facilitating chromosome segregation. Both BLM and PICH undergo transient mitotic hyper-phosphorylation, but the biological significance of this remains elusive. Here, we uncover that during early mitosis, multiple protein kinases act together to strictly constrain BTRR complex activities at centromeres. Mechanistically, CDK1 destabilises the complex and suppresses its association with PICH at the chromatin underneath kinetochores. Inactivating the BLM and TOP3A interaction compromises the UFB-binding complex mitotic functions and can prevent centromere destruction. We further unravel how different mitotic phosphorylation sites of BLM affect its interaction with the TOP3A/RMI1/RMI2 subcomplex and centromeric DNA unwinding. Furthermore, we show that multiple PLK1-mediated phosphorylation on BLM is required to suppress aberrant centromere unwinding. However, notably, unleashing such activity after sister-chromatid cohesion loss facilitates separation of entangled chromosomes. Together, our study defines a centromere protection pathway in human mitotic cells, heavily reliant on a tight spatiotemporal control of the BTRR complex.

2025-08-12 | PXD064192 | Pride

BLM complex composition in unperturbed cells

Project description:The Bloom syndrome DNA helicase BLM contributes to chromosome stability through its roles in double-strand break repair by homologous recombination and DNA replication fork restart during the replication stress response. Loss of BLM activity leads to Bloom syndrome, which is characterized by extraordinary cancer risk and small stature. Here, we have analyzed the composition of the BLM complex in unperturbed cells and identified a direct physical interaction with the Mcm6 subunit of the minichromosome maintenance (MCM) complex by co-immunopecipitations using endogenous and recombinant proteins as well as two-hybrid analysis.

2022-02-15 | PXD018823 | Pride

Tianlongkechuanling Inhibits Pulmonary Fibrosis Through Down-Regulation Of Arginase-Ornithine Pathway

Project description:Background: Pulmonary Fibrosis (PF) is an interstitial lung disease of unknown etiology, characterized by excessive accumulation of extracellular matrix in the lungs, which disrupts the structure and gas exchange of the alveoli. There are only two approved therapies for PF, nintedanib (Nib) and pirfenidone. Therefore, the use of Chinese medicine for PF is attracting attention. Tianlongkechuanling (TL) is an effective Chinese formula that has been applied clinically to alleviate PF, which can enhance lung function and quality of life. Purpose: The potential effects and specific mechanisms of TL have not been fully explored, yet. In the present study, proteomics was performed to explore the therapeutic protein targets of TL on Bleomycin (BLM)-induced Pulmonary Fibrosis. Method: BLM-induced PF mice models were established. Hematoxylineosin staining and Masson staining were used to analyze histopathological changes and collagen deposition. To screen the differential proteins expression between the Control, BLM, BLM+TL and BLM+ Nib (BLM+ Nintedanib) groups, quantitative proteomics was performed using tandem mass tag (TMT) labeling with nanoLC-MS/MS [nano liquid chromatographymass spectrometry]). Changes in the profiles of the expressed proteins were analyzed using the bioinformatics tools Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). The protein–protein interactions (PPI) were established by STRING. Expressions of α-smooth muscle actin (α-SMA), Collagen I (Col1a1), Fibronectin (Fn1) and enzymes in arginase-ornithine pathway were detected by Western blot or RT-PCR.

2021-09-10 | PXD024058 | Pride

SCGB3A2 suppresses bleomycin-induced pulmonary fibrosis through activation of STAT1 and up-regulation of SMAD7

Project description:We report for the first time that secretoglobin (SCGB) 3A2, a novel cytokine-like molecule, predominantly expressed in pulmonary airways epithelium, drastically reduced the severity of lung fibrosis using bleomycin-induced mouse model. DNA microarrays were performed using RNAs isolated from mouse lungs in two experiments. In the first experiments, mice were adminitered intravenously SCGB3A2 or PBS once daily for a week, starting on day 14 after BLM administration, and in the second experiments, SCGB3A2 or PBS was administered intravenously for 12 hrs.

2011-04-30 | E-GEOD-21560 | biostudies-arrayexpress

ChIP Sequencing of CRISPR/Cas9 corrected Bloom Syndrome patient cell line using antibody against BLM

Project description:BLM protein has been shown to play an important role in homologous recombination (HR) repair. We report that BLM interacts with RAD54 (another HR repair protein) to enhance its chromatin remodeling function. This experiment identifies that BLM gets recruited to different genetic loci even in the absence of damage, possibly along with RAD54 chromatin remodeler.

2024-04-03 | E-MTAB-11372 | biostudies-arrayexpress

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