ArticleProteome science2019
The interactome and proteomic responses of ALKBH7 in cell lines by in-depth proteomics analysis.
Article in Proteome science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- LIN28A-Dependent Kinome and Phosphoproteome Reprogramming Promotes Imatinib Resistance.Molecular & cellular proteomics : MCP · 2026Article
- Integrative pan-cancer analysis reveals the prognostic and immunotherapeutic value of ALKBH7 in HNSC.Aging · 2024Article
- Genetic alterations in juvenile cervical clear cell adenocarcinoma unrelated to human papillomavirus.Frontiers in medicine · 2023Article
- A Pan-Cancer Analysis Reveals the Prognostic and Immunotherapeutic Value of ALKBH7.Frontiers in genetics · 2022Article
- Association of a Novel DOCK2 Mutation-Related Gene Signature With Immune in Hepatocellular Carcinoma.Frontiers in genetics · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundALKBH7 is a mitochondrial protein, involved in programmed necrosis, fatty acid metabolism, cell cycle regulation, and prostate cancer disease. However, the exact roles of ALKBH7 and the underlying molecular mechanisms remain mysterious. Thus, investigations of the interactome and proteomic responses of ALKBH7 in cell lines using proteomics strategies are urgently required.
methodsIn the present study, we investigated the interactome of ALKBH7 in mitochondria through immunoprecipitation-mass spectrometry/mass spectrometry (IP-MS/MS). Additionally, we established the ALKBH7 knockdown and overexpression cell lines and further identified the differentially expressed proteins (DEPs) in these cell lines by TMT-based MS/MS. Two DEPs (UQCRH and HMGN1) were validated by western blotting analysis.
resultsThrough bioinformatic analysis the proteomics data, we found that ALKBH7 was involved in protein homeostasis and cellular immunity, as well as cell proliferation, lipid metabolism, and programmed necrosis by regulating the expression of PTMA, PTMS, UQCRH, HMGN1, and HMGN2. Knockdown of ALKBH7 resulted in upregulation of UQCRH and HMGN1 expression, and the opposite pattern of expression was detected in ALKBH7 overexpression cell lines; these results were consistent with our proteomics data.
conclusionOur findings indicate that the expression of UQCRH and HMGN1 is regulated by ALKBH7, which provides potential directions for future studies of ALKBH7. Furthermore, our results also provide comprehensive insights into the molecular mechanisms and pathways associated with ALKBH7.
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