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Lnc1267 binding proteins were identified by mass spectrometry.

ABSTRACT: In this study, we used mass spectrometry to analyze lnc1267 interacting proteins. Firstly, the lnc1267 interacting protein was pulled down by RNA pull-down experiment, then the protein sample was separated by silver staining, and finally the differential protein bands were analyzed by Shotgun mass spectrometry. Based on the mass spectrometry data, we selected high score binding proteins for further verification. This process helps uncover function and molecular mechanism of lnc1267.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Hela Cell

SUBMITTER: ying Fan

LAB HEAD: Zhidong Wang

PROVIDER: PXD060717 | Pride | 2026-03-02

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	FL2-1.msf	Msf
	FL2-1.raw	Raw
	FL2-2.msf	Msf
	FL2-2.raw	Raw
	FL2-3.msf	Msf

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1 - 5 of 13

Publications

Lnc1267-hnRNP U interaction promotes radioresistance by inhibiting apoptosis via attenuated RelA/p65 Ser536 phosphorylation.

Qi Zhenhua Z Fan Ying Y Liu Xin X Cai Dan D Lin Chuxian C Li Yaqiong Y Zhang Hong H Jia Meng M Han Jixia J Mo Yunqi Y Zhu Maoxiang M Shen Liping L Wang Qi Q Wang Zhidong Z

Cellular and molecular life sciences : CMLS 20260217 1

Radiotherapy efficacy is frequently limited by tumor radioresistance, with dysregulated apoptosis playing a pivotal role. While NF-κB is a well-established mediator of cancer radioresistance (primarily through anti-apoptotic mechanisms), the paradoxical pro-apoptotic function of radiation-induced NF-κB activation remains poorly understood. Emerging evidence suggests that certain conserved lncRNAs may function analogously to housekeeping genes during tumor progression; however, their involvement ...[more]

PMID: 41703117

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Identification the proteins interacted with SNHG26 in human keratinocytes

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2024-08-28 | PXD055231 | Pride

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Proteins binding in vitro to normal and mutant FMR1 5'UTR mRNA

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2025-11-21 | PXD053905 | Pride

lnc-EAPV binding proteins in C57BL/6J BMDMs

Project description:Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.

2018-11-07 | PXD011577 | Pride

Identification of interaction partners of the lncRNA Pantr1

Project description:Derailed gene expression programs within the developing nervous system, encompassing both transcriptional and posttranscriptional processes, can cause diverse neurodevelopmental diseases (NDD). The NDD FOXG1-syndrome lacks full understanding of the mechanistic role of its eponymous gene product. While it is known that FOXG1 acts in part at the chromatin by binding to regulative regions, it is unclear what factors control its presence at specific sites. Long non-coding RNAs (lncRNAs) can mediate site-directed transcription factor binding, but their potential role in FOXG1-syndrome has not been described. Here, we show that FOXG1 localisation is regulated at selected loci through the lncRNA Pantr1. We identified FOXG1 as an upstream transcriptional activator of Pantr1 in human and mice. Further, we discovered that FOXG1 has the ability to associate with RNAs. Both, transcriptional regulation of Pantr1 by FOXG1 and association of both partners, build up a regulative network that impacts the localisation of FOXG1 at selected genomic loci. Specifically, Pantr1 facilitates cooperative presence of FOXG1/NEUROD1 at specific sites, and Pantr1 reduction leads to redistribution of FOXG1 to comparably more generic binding sites. The rescue of impaired dendritic outgrowth upon FOXG1 reduction by simultaneous overexpression of Pantr1 underlines the importance of the FOXG1/Pantr1 regulative network.

2025-06-03 | PXD056060 | Pride

Proteomics analysis of lncRNA ZNF252P interacting proteins in A549 cell line

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2025-01-18 | PXD053695 | Pride

Silver nano-colloids disrupt medaka embryogenesis through vital gene expressions

Project description:Using medaka fish embryo model, toxic effects of silver nanocolloids (SNC, 3.8M-BM-11.0nm diameter) on developmental morphology and gene expression profile were investigated. SNC caused morphological changes in embryos including cardiovascular malformations, ischemia, underdeveloped central nervous system and eyes, and kyphosis at exposures of 0.5mg/L and 1.0mg/L.. To determine in vivo distribution of SNC, medaka embryos were exposed to 0.5mg/L for 6 days and subjected to ICP-OES analyses. Silver was detected in medaka embryos and chorion at levels of 16.6M-BM-19.3pg and 720M-BM-129pg, respectively. TEM analyses showed SNC adhered to the chorion surface and inside the chorion. On investigation of oxidative mechanism, NAC (0.05mM) rescued all embryos by 96-hr post treatment, while 0.5mM GSH did not. NAC blocked lipid peroxidation. Furthermore, medaka oligo DNA microarray and qRT-PCR were used for gene expression profiling in embryos exposed for 48-hr to 0.05mg/L SNC. Six genes relative to embryogenesis and morphogenesis such as ctsL, Tpm1, RBP, mt, atp2a1 and hox6b6 turned out to be affected and their involvement to the above malformations was implied. In conclusion, SNC causes gross malformations in the cardiovascular and central nervous systems in developing medaka embryos through potentially SNC-affected differential expression of a series of genes related to oxidative stress, embryonic cellular proliferation, and morphological development. Three of the stage-21 medaka embryos per sample were exposed in triplicate to 0mg/L (control) and 0.05mg/L SNC for 48 hours. Therefore, for each exposure condition nine of the stage-21 embryos were prepared and used in the SNC exposure test.

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Long non-coding RNA HOTTIP promotes CCL3 expression and induces cartilage degradation by sponging miR-455-3p

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