Mohammad Omar Faruk
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Mohammad Omar Faruk has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Masaaki Komatsu
Department of Physiology, Juntendo University Graduate School of Medicine, Tokyo, Japan
2 shared publications - Yoshinobu Ichimura
Department of Physiology, Juntendo University Graduate School of Medicine
2 shared publications - Afnan H. El-Gowily
Biochemistry Division, Department of Chemistry, Faculty of Science, Tanta University, Tanta 31527, Egypt
1 shared publication Masato Koike
Department of Cell Biology and Neuroscience, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan
1 shared publication- Nobuo N. Noda
Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan
1 shared publication Satoko Komatsu-Hirota
Department of Physiology, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan
1 shared publication
Latest Publications
- Open Access
- 12 November 2021
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 297 (6) , 101405
Phase-separated protein droplets of amyotrophic lateral sclerosis-associated p62/SQSTM1 mutants show reduced inner fluidity
- 12 November 2021
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 297 (6) , 101405
Open AccessPhase-separated protein droplets of amyotrophic lateral sclerosis-associated p62/SQSTM1 mutants show reduced inner fluidity
- Open Access
- 18 August 2021
- Published by Wiley in Cancer Science
- Vol. 112 (10) , 3972-3978
Selective autophagy
While starvation‐induced autophagy is thought to randomly degrade cellular components, under certain circumstances autophagy selectively recognizes, sequesters, and degrades specific targets via autophagosomes. This process is called selective autophagy, and it contributes to cellular homeostasis by degrading specific soluble proteins, supramolecular complexes, liquid‐liquid phase‐separated droplets, abnormal or excess organelles, and pathogenic invasive bacteria. This means that autophagy, like the ubiquitin‐proteasome system, strictly regulates diverse cellular functions through its selectivity. In this short review, we focus on the mechanism of "selective" autophagy, which is rapidly being elucidated.
- 18 August 2021
- Published by Wiley in Cancer Science
- Vol. 112 (10) , 3972-3978
Open AccessSelective autophagy
While starvation‐induced autophagy is thought to randomly degrade cellular components, under certain circumstances autophagy selectively recognizes, sequesters, and degrades specific targets via autophagosomes. This process is called selective autophagy, and it contributes to cellular homeostasis by degrading specific soluble proteins, supramolecular complexes, liquid‐liquid phase‐separated droplets, abnormal or excess organelles, and pathogenic invasive bacteria. This means that autophagy, like the ubiquitin‐proteasome system, strictly regulates diverse cellular functions through its selectivity. In this short review, we focus on the mechanism of "selective" autophagy, which is rapidly being elucidated.