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ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [UV-CLIP_ZCCHC4]

ABSTRACT: ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [UV-CLIP_ZCCHC4]

PROVIDER: PRJNA779970 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16930721.fastq.gz	Fastqsanger.gz
	SRR16930722.fastq.gz	Fastqsanger.gz

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ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [UV-CLIP_ZCCHC4]

Project description:Purpose: We performed UV-CLIP-seq to investigate the RNAs interacting with ZCCHC4. The goal of this study is to investigate the role of ZCCHC4 in regulating the progression and prognosis of HCC. We have found that ZCCHC4 could inhibit DNA damage agent induced DNA damage and apoptosis of HCC, and promote chemoresistance. We proposed that ZCCHC4 could interact with RNAs to regulate chemoresistance.

2022-07-27 | GSE188703 | GEO

ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma

Project description:ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma

| PRJNA779966 | ENA

ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO]

Project description:ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO]

| PRJNA779967 | ENA

ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO OXA]

Project description:ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO OXA]

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ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO]

Project description:Purpose: We performed RNA sequencing (RNA-seq) analysis of ZCCHC4 KO1 cells and wild type cells to find differentially expressed genes regulated by ZCCHC4 in HCC cells. The goal of this study is to investigate the biological effect of ZCCHC4 in HCC progression and prognosis.

2022-07-27 | GSE188702 | GEO

ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO OXA]

Project description:Purpose: We performed RNA sequencing (RNA-seq) analysis to investigate the role of ZCCHC4 in regulating OXA-induced genes in HepG2 cells. The goal of this study is to investigate the biological effect of ZCCHC4 in HCC progression and prognosis, and we have found that ZCCHC4 could promote chmoresistance of HCC to DNA damage agents including OXA, we conducted RNA-seq to figure out more clues for deep mechanisms.

2022-07-27 | GSE190632 | GEO

ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-27 | GSE188704 | GEO

A new N6-methyladenosine methyltransferase ZCCHC4 mediates rRNA methylation and mRNA interaction

Project description:N6-methyladenosine (m6A) plays critical roles in a wide range of physiological and pathological processes, and m6A methyltransferases are still being discovered for different RNA species in mammals. Here report a new m6A methyltransferase ZCCHC4 that methylates ribosomal RNA (rRNA) and interacts with messenger RNA (mRNA), ZCCHC4 has methylation activity on rRNA with a preference for AAC consensus sequence. ZCCHC4 can affect global translation through m6A methylation, mostly on 28S rRNA.

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Whole-genome landscape of histone H2AX and γ-H2AX

Project description:Phosphorylation of the histone variant H2AX forms γ-H2AX that marks DNA double-strand break (DSB). Here we generated the sequencing-based maps of H2AX and γ-H2AX positioning in resting and proliferating cells before and after ionizing irradiation. Genome-wide locations of possible endogenous and exogenous DSBs were identified based on γ-H2AX distribution in dividing cancer cells without irradiation and that in resting cells upon irradiation, respectively. γ-H2AX-enriched regions of endogenous origin in replicating cells included telomeres and active transcription start sites, apparently reflecting replication- and transcription-mediated stress during rapid cell division. Surprisingly, H2AX itself, prior to phosphorylation, was specifically located at these endogenous hotspots. This phenomenon was only observed in dividing cancer cells but not in resting cells. Endogenous H2AX was concentrated on the transcription start site of actively transcribed genes but was irrelevant to pausing of RNA polymerase II (pol II), which precisely coincided with γ-H2AX of endogenous origin. γ-H2AX enrichment upon irradiation also coincided with actively transcribed regions, but unlike endogenous γ-H2AX, it extended into the gene body and was not specifically concentrated on the pausing site of pol II. Subtelomeres were not responsive to external DNA damage. Our findings provide insight into DNA repair programs of cancer and may have implications for cancer therapy.

2012-04-04 | GSE25577 | GEO

Whole-genome landscape of histone H2AX and γ-H2AX along with related factors in activated cells

Project description:Phosphorylation of the histone variant H2AX forms γ-H2AX, which serves as a marker of DNA repair response. Here we provide ChIP-seq-based maps of histone H2AX, γ-H2AX, H2AZ, INO80, SRCAP, and RNA polymerase II in activated T cells. Matched data for H2AX and γ-H2AX in resting T cells and Jurkat cancer T cells are available in GSE25577.

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