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Updated: Nov 9, 2025
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Study of Protein-protein Interactions in Autophagy Research
Published on: September 9, 2017
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Nlp promotes autophagy through facilitating the interaction of Rab7 and FYCO1
Wenchang Xiao1,2, Danna Yeerken3, Jia Li1
1State Key Laboratory of Molecular Oncology, National Cancer center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Signal Transduction and Targeted Therapy
|April 16, 2021
Summary
Ninein-like protein (Nlp) regulates autophagy by promoting autophagosome transport. Nlp deficiency in mice increases liver cancer risk due to impaired autophagy.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Autophagy is crucial for cellular homeostasis and preventing cancer.
- Autophagosome transport mechanisms are not fully understood.
- Ninein-like protein (Nlp) is a known centrosomal protein.
Purpose of the Study:
- To investigate the role of Nlp in autophagy.
- To elucidate the mechanism by which Nlp affects autophagosome transport.
Main Methods:
- Co-localization studies of Nlp with autophagosomes and autophagy markers (LC3, Rab7, FYCO1).
- Interaction assays to determine Nlp's effect on Rab7-FYCO1 binding.
- Analysis of liver cancer incidence and autophagic defects in Nlp-deficient mice.
Main Results:
- Nlp colocalizes with autophagosomes and interacts with LC3, Rab7, and FYCO1.
- Nlp enhances the interaction between Rab7 and FYCO1, accelerating autophagic flux.
- Nlp deficiency in mice leads to impaired autophagy, increased hepatomegaly, and liver cancer incidence.
Conclusions:
- Nlp is a novel regulator of autophagy, distinct from its known centrosomal functions.
- Nlp facilitates autophagolysosome formation by promoting Rab7-FYCO1 interaction.
- Nlp plays a protective role against liver cancer development by maintaining autophagic function.
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