A5052867383- Autophagy in Disease and Therapy
- Polyamine Metabolism and Applications
- Plant Gene Expression Analysis
- Endoplasmic Reticulum Stress and Disease
- Signaling Pathways in Disease
- Extracellular vesicles in disease
- Epigenetics and DNA Methylation
- CRISPR and Genetic Engineering
- Fungal Biology and Applications
- RNA Research and Splicing
- Studies on Chitinases and Chitosanases
- Fuel Cells and Related Materials
- RNA modifications and cancer
- Phagocytosis and Immune Regulation
- Quinazolinone synthesis and applications
- Parkinson's Disease Mechanisms and Treatments
- Fungal and yeast genetics research
UCSF Helen Diller Family Comprehensive Cancer Center
2016-2021
University of California, San Francisco
2016-2021
University of California, Davis
2012-2017
The yeast AGC kinase orthologs Ypk1 and Ypk2 control several important cellular processes, including actin polarization, endocytosis, sphingolipid metabolism. Activation of Ypk1/2 requires phosphorylation by kinases localized at the plasma membrane (PM), 3-phosphoinositide-dependent 1 Pkh1/Pkh2 target rapamycin complex 2 (TORC2). Unlike their mammalian counterparts SGK Akt, lack an identifiable lipid-targeting motif; therefore, how these proteins are recruited to PM has remained elusive. To...
Significance Autophagy recycles cytoplasmic components to facilitate cellular homeostasis and adaptation in response nutrient deprivation. Impaired autophagy regulation is linked numerous metabolic aging-related disorders. One important regulator of the Target Rapamycin (TOR) kinase, which assembles into two complexes: TOR Complex 1 (TORC1) 2 (TORC2), where TORC1 a well-established negative autophagy. Here we characterize pathway wherein TORC2 its downstream target Ypk1, act as positive...
The conserved target of rapamycin (TOR) kinase is a central regulator cell growth in response to nutrient availability. TOR forms 2 structurally and functionally distinct complexes, TORC1 TORC2, negatively regulates autophagy via TORC1. Here we demonstrate also operates independently through the TORC2 signaling pathway promote upon amino acid limitation. Under these conditions, its downstream Ypk1, inhibits Ca2+- Cmd1/calmodulin-dependent phosphatase, calcineurin, enable activation...
Macroautophagy/autophagy is a starvation and stress-induced catabolic process critical for cellular homeostasis adaptation. Several Atg proteins are involved in the formation of autophagosome subsequent degradation cytoplasmic components, termed autophagy flux. Additionally, expression several proteins, particular Atg8, modulated transcriptionally, yet regulatory mechanisms remain poorly understood. Here we demonstrate that AGC kinase Ypk1, target rapamycin-insensitive TORC2 signaling...
Autophagy is a catabolic process that recycles cytoplasmic contents and crucial for cell survival during stress. The target of rapamycin (TOR) kinase regulates autophagy as part two distinct protein complexes, TORC1 TORC2. negatively according to nitrogen availability. In contrast, TORC2 functions positive regulator amino acid starvation, via its Ypk1, by repressing the activity calcium-dependent phosphatase calcineurin promoting general control (GAAC) response. Precisely how TORC2-Ypk1...
The target of rapamycin (TOR) kinase is a conserved regulator cell growth and functions within 2 different protein complexes, TORC1 TORC2, where TORC2 positively controls macroautophagy/autophagy during amino acid starvation. Under these conditions, signaling inhibits the activity calcium-regulated phosphatase calcineurin promotes general control (GAAC) response autophagy. Here we demonstrate that regulates by controlling respiratory mitochondria. In particular, find mitochondrial oxidative...
In Saccharomyces cerevisiae, the selective autophagic degradation of mitochondria, termed mitophagy, is critically regulated by adapter protein Atg32. Despite our knowledge about molecular mechanisms which Atg32 controls its physiological roles in yeast survival and fitness remains less clear. Here, we demonstrate a requirement for promoting spermidine production during respiratory growth heat-induced mitochondrial stress. During growth, mitophagy-deficient exhibit profound heat-stress...