ArticleScientific reports2020
Human ZKSCAN3 and Drosophila M1BP are functionally homologous transcription factors in autophagy regulation.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Research Progress on the Functional Regulation Mechanisms of ZKSCAN3.Biomolecules · 2025Review
- Drosophila architectural proteins M1BP and Opbp cooperatively form the active promoter of a ribosomal protein gene.Epigenetics & chromatin · 2025Article
- The Biological Roles of ZKSCAN3 (ZNF306) in the Hallmarks of Cancer: From Mechanisms to Therapeutics.International journal of molecular sciences · 2024Review
- M1BP is an essential transcriptional activator of oxidative metabolism during Drosophila development.Nature communications · 2023Article
- Association between autophagy and acute pancreatitis.Frontiers in genetics · 2023Review
- Transcriptional pausing factor M1BP regulates cellular homeostasis by suppressing autophagy and apoptosis inAutophagy reports · 2023Article
- Association ofFrontiers in genetics · 2022Article
- Transcription and Post-translational Regulation of Autophagy in Insects.Frontiers in physiology · 2022Article
- CHD1L augments autophagy-mediated migration of hepatocellular carcinoma through targeting ZKSCAN3.Cell death & disease · 2021Article
- An RNA-interference screen in Drosophila to identify ZAD-containing C2H2 zinc finger genes that function in female germ cells.G3 (Bethesda, Md.) · 2021Article
- Overexpression of ZNF460 predicts worse survival and promotes metastasis through JAK2/STAT3 signaling pathway in patient with colon cancer.Journal of Cancer · 2021Article
- Motif 1 Binding Protein suppresses wingless to promote eye fate in Drosophila.Scientific reports · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is an essential cellular process that maintains homeostasis by recycling damaged organelles and nutrients during development and cellular stress. ZKSCAN3 is the sole identified master transcriptional repressor of autophagy in human cell lines. How ZKSCAN3 achieves autophagy repression at the mechanistic or organismal level however still remains to be elucidated. Furthermore, Zkscan3 knockout mice display no discernable autophagy-related phenotypes, suggesting that there may be substantial differences in the regulation of autophagy between normal tissues and tumor cell lines. Here, we demonstrate that vertebrate ZKSCAN3 and Drosophila M1BP are functionally homologous transcription factors in autophagy repression. Expression of ZKSCAN3 in Drosophila prevents premature autophagy onset due to loss of M1BP function and conversely, M1BP expression in human cells can prevent starvation-induced autophagy due to loss of nuclear ZKSCAN3 function. In Drosophila ZKSCAN3 binds genome-wide to sequences targeted by M1BP and transcriptionally regulates the majority of M1BP-controlled genes, demonstrating the evolutionary conservation of the transcriptional repression of autophagy. This study thus allows the potential for transitioning the mechanisms, gene targets and plethora metabolic processes controlled by M1BP onto ZKSCAN3 and opens up Drosophila as a tool in studying the function of ZKSCAN3 in autophagy and tumourigenesis.
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