A5057383431- Autophagy in Disease and Therapy
- Genetics, Aging, and Longevity in Model Organisms
- Mitochondrial Function and Pathology
- Pancreatic function and diabetes
- Endoplasmic Reticulum Stress and Disease
- Metabolism, Diabetes, and Cancer
- Lipid metabolism and biosynthesis
- MicroRNA in disease regulation
- Gene expression and cancer classification
- Genomics, phytochemicals, and oxidative stress
- Structural Health Monitoring Techniques
- Protein Hydrolysis and Bioactive Peptides
- Biochemical Acid Research Studies
- Machine Learning in Bioinformatics
- Bioinformatics and Genomic Networks
- Machine Fault Diagnosis Techniques
- Cancer, Hypoxia, and Metabolism
- Protein Tyrosine Phosphatases
- Hippo pathway signaling and YAP/TAZ
- Image and Signal Denoising Methods
- Aquaculture Nutrition and Growth
- Topic Modeling
- Non-Destructive Testing Techniques
- Sirtuins and Resveratrol in Medicine
- Apelin-related biomedical research
State Key Laboratory of Genetic Engineering
2023-2025
Fudan University
2023-2025
École Polytechnique Fédérale de Lausanne
2019-2024
Xiamen University
2013-2023
Weatherford College
2020
Chuxiong Normal University
2020
Google (United States)
2018
In metazoans, cells depend on extracellular growth factors for energy homeostasis. We found that glycogen synthase kinase-3 (GSK3), when deinhibited by default in deprived of factors, activates acetyltransferase TIP60 through phosphorylating TIP60-Ser(86), which directly acetylates and stimulates the protein kinase ULK1, is required autophagy. Cells engineered to express TIP60(S86A) cannot be phosphorylated GSK3 could not undergo serum deprivation-induced An acetylation-defective mutant ULK1...
The transcriptional coactivator Yes-associated protein (YAP) plays an important role in organ-size control and tumorigenesis. However, how Yap gene expression is regulated remains unknown. This study shows that the Ets family member GABP binds to promoter activates YAP transcription. depletion of downregulates YAP, resulting a G1/S cell-cycle block increased cell death, both which are substantially rescued by reconstituting YAP. can be inactivated oxidative mechanisms, acetaminophen-induced...
Obesity is characterized by excessive fatty acid conversion to triacylglycerols (TAGs) in adipose tissues. However, how signaling networks sense acids and connect the stimulation of lipid synthesis remains elusive. Here, we show that homozygous knock-in mice carrying a point mutation at Ser86 phosphorylation site acetyltransferase Tip60 (Tip60 SA/SA ) display remarkably reduced body fat mass, females fail nurture pups adulthood due severely milk TAGs. Mechanistically, stimulate...
Abstract Increased lipogenesis has been linked to an increased cancer risk and poor prognosis; however, the underlying mechanisms remain obscure. Here we show that phosphatidic acid phosphatase (PAP) lipin-1, which generates diglyceride precursors necessary for synthesis of glycerolipids, interacts with is a direct substrate Src proto-oncogenic tyrosine kinase. Obesity-associated microenvironmental factors other Src-activating growth factors, including epidermal factor, activate promote...
Mitohormesis defines the increase in fitness mediated by adaptive responses to mild mitochondrial stress. Tetracyclines inhibit not only bacterial but also translation, thus imposing a low level of stress on eukaryotic cells. We demonstrate cell and germ-free mouse models that tetracyclines induce response (MSR), involving both ATF4-mediated integrative type I interferon (IFN) signaling. To overcome interferences with host microbiome, we identify tetracycline derivatives have minimal...
Lysosomes are central platforms for not only the degradation of macromolecules but also integration multiple signaling pathways. However, whether and how lysosomes mediate mitochondrial stress response (MSR) remain largely unknown. Here, we demonstrate that lysosomal acidification via vacuolar H+-ATPase (v-ATPase) is essential transcriptional activation unfolded protein (UPRmt). Mitochondrial stimulates v-ATPase-mediated mechanistic target rapamycin complex 1 (mTORC1), which then directly...
Hypoxia-inducible factors (HIFs) are master regulators of adaptive responses to low oxygen, and their α-subunits rapidly degraded through the ubiquitination-dependent proteasomal pathway after hydroxylation. Aberrant accumulation or activation HIFs is closely linked many types cancer. However, how hydroxylation HIFα its delivery ubiquitination machinery regulated remains unclear. Here we show that Rho-related BTB domain-containing protein 3 (RHOBTB3) directly interacts with hydroxylase PHD2...
The functions of many eukaryotic genes are still poorly understood. Here, we developed and validated a new method, termed GeneBridge, which is based on two linked approaches to impute gene function bridge with biological processes. First, G ene- M odule A ssociation D etermination (G-MAD) allows the annotation function. Second, odule- (M-MAD) predicting connectivity among modules. We applied GeneBridge tools large-scale multispecies expression compendia—1700 data sets over 300,000 samples...
Abstract The male’s ability to reproduce is completely dependent on Sertoli cells. However, the mechanisms governing functional integrity of cells have remained largely unexplored. Here, we demonstrate that deletion Shp2 in results infertility mice. In knockout mice (SCSKO), a normal population was observed, but blood-testis barrier (BTB) not formed. ablation initiated untimely and excessive differentiation spermatogonial stem (SSCs) by disturbing expression paracrine factors. As...
Analysis of circulating tumor cells (CTCs) is regarded as a useful diagnostic index to monitor development and guide precision medicine. Although the immunoassay common strategy for CTC identification heterogeneity characterization, it challenged by poor reaction efficiency laborious manipulations in microdevices, which hinder sensitivity, throughput, simplification, applicability. To meet need rapid, sensitive, simple analysis, we developed an efficient detection system integrating 3D...
unc-51-like autophagy activating kinase 1 and 2 (Ulk1/2) regulate initiation under various stress conditions. However, the physiological functions of these Ser/Thr kinases are not well characterized. Here, we show that mice with liver-specific double knockout (LDKO) Ulk1 Ulk2 (Ulk1/2 LDKO) viable, but exhibit overt hepatomegaly phenotype. Surprisingly, Ulk1/2 LDKO display normal autophagic activity in hepatocytes upon overnight fasting, strongly resistant to acetaminophen (APAP)-induced...
Mitochondrial function is critical for neuronal activity and systemic metabolic adaptation. In this issue, Li et al. (https://doi.org/10.1083/jcb.202408050) identify TMBIM-2 as a key regulator of calcium dynamics, coordinating the neuronal-to-intestinal mitochondrial unfolded protein response (UPRmt), pathogen-induced aversive learning, aging.
To adapt mitochondrial function to the ever-changing intra- and extracellular environment, multiple stress response (MSR) pathways, including unfolded protein (UPRmt), have evolved. However, how signal is sensed relayed UPRmt transcription factors, such as ATFS-1 in Caenorhabditis elegans, remains largely unknown. Here, we show that a panel of vacuolar H+-ATPase (v-ATPase) subunits target rapamycin complex 1 (TORC1) activity are essential for cytosolic relay induction UPRmt. Mechanistically,...