FIP200, a key signaling node to coordinately regulate various cellular processes
Open accessAbstract
A central question in cell biology is how various cellular processes are coordinately regulated in normal cell and how dysregulation of the normal signaling pathways leads to diseases such as cancer. Recent studies have identified FIP200 as a crucial signaling component to coordinately regulate different cellular events by its interaction with multiple signaling pathways. This review will focus on the cellular functions of FIP200 and its interacting proteins, as well as the emerging roles of FIP200 in embryogenesis and cancer development. Further understanding of FIP200 function might provide novel therapeutic targets for human diseases such as cancer.
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RB1CC1 is also important in regulating intracellular signaling pathways such as cell survival, differentiation, migration, proliferation, and protein synthesis.
“Aside from the essential function of RB1CC1 in regulating autophagy in mammalian cells, it is also important in regulating a number of intracellular signaling pathways such as cell survival, differentiation, migration, proliferation, and protein synthesis. 38”
From Deletion of autophagy inducer <i>RB1CC1</i> results in degeneration of the retinal pigment epithelium (2015) · cites this paper as [38]
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References 60 · Cited by 67
- Authors
- Gan, B., & Guan, J.-L.
- Affiliations
- Harvard University (US)
- University of Michigan (US)
- Corresponding author
- Guan, Jun-Lin
- Venue
- Cellular Signalling
- Publisher
- Elsevier BV
- Published
- 2008-05
- Volume
- 20
- Issue
- 5
- Pages
- 787-794
- ISSN
- 0898-6568 (ISSN-L)
- PMC
- PMC2278039
- OpenAlex
- W1985193239
- Cited by
- 67
- References
- 60
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 5 · 2020: 5 · 2019: 2 · 2018: 3 · 2017: 2 · 2016: 7 · 2015: 5 · 2014: 4 · 2013: 5 · 2012: 3
- FWCI
- 0.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cellular Signalling (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (GM52890, R01GM052890)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Keywords
- FIP200, protein-protein interaction, embryonic development, carcinogenesis, cancer therapy targets, cell regulation
- MeSH terms
- Autophagy-Related Proteins, Animals, Cell Differentiation, Cell Movement, Cell Survival, Female, Humans, Models, Biological, Neoplasms, Pregnancy, Protein-Tyrosine Kinases, Protein Biosynthesis, Signal Transduction, Gene Expression, Mice, Knockout, Embryonic Development, Intracellular Signaling Peptides and Proteins, Cell Proliferation, Mice
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