A5065612522- Mitochondrial Function and Pathology
- Autophagy in Disease and Therapy
- Kruppel-like factors research
- Immune Cell Function and Interaction
- Wnt/β-catenin signaling in development and cancer
- Cancer-related Molecular Pathways
- Cancer, Hypoxia, and Metabolism
- Sirtuins and Resveratrol in Medicine
- Genetic factors in colorectal cancer
- Immunotherapy and Immune Responses
- Wound Healing and Treatments
- RNA modifications and cancer
- High Altitude and Hypoxia
- Silk-based biomaterials and applications
- Immune cells in cancer
- Eating Disorders and Behaviors
- Hemoglobin structure and function
- Cancer Immunotherapy and Biomarkers
- Cardiovascular Disease and Adiposity
- Nitric Oxide and Endothelin Effects
- Histone Deacetylase Inhibitors Research
- Genomics, phytochemicals, and oxidative stress
- Cancer-related gene regulation
- Atherosclerosis and Cardiovascular Diseases
- Endoplasmic Reticulum Stress and Disease
Boston Children's Hospital
2018-2025
Boston Children's Museum
2025
Harvard University
2023
Albert Einstein College of Medicine
2015-2021
Boston Medical Center
2021
China Medical University
2018
CAO Group (United States)
2017
University of Zurich
2016
National Institutes of Health
2009
National Institute of Diabetes and Digestive and Kidney Diseases
2009
Both the stress-response protein, SIRT1, and cell cycle checkpoint kinase, CHK2, play critical roles in aging cancer via modulation of cellular homeostasis maintenance genomic integrity. However, underlying mechanism linking two pathways remains elusive. Here, we show that SIRT1 functions as a modifier CHK2 control. Specifically, interacts with deacetylates it at lysine 520 residue, which suppresses phosphorylation, dimerization, thus activation. depletion induces hyperactivation-mediated...
Metabolic reprogramming is a distinct hallmark in tumorigenesis. Autophagy can rewire cell metabolism by regulating intracellular homeostasis. Warburg effect specific energy metabolic process that allows tumor cells to metabolize glucose via glycolysis into lactate even the presence of oxygen. Although both autophagy and are involved stress response crisis cells, their molecular relationship has remained largely elusive. We found Atg7, key molecule autophagy, inhibits effect....
SIRT2-mediated deacetylation of SMC1A promotes its phosphorylation and overcomes the oncogenic stress for tumor cell survival.
Abstract Beyond personal hygiene, the most impactful public health innovation in human history has been development of vaccines to protect against lethal infections. Cancer have long-been envisioned, with minimal clinical success. Hepatocellular carcinoma (HCC) is common liver tumor and one leading causes cancer-related mortality worldwide. Unfortunately, HCC patients fail respond widely used T-cell based immunotherapies, likely due relatively immunotolerant nature disease. Thus, there an...
Environmental and genetic factors are important both in affecting life span neoplastic transformation. We have shown previously that mice, which homozygous for full-length breast cancer-associated gene-1 (Brca1) deletion heterozygous a p53-null mutation (Brca1Δ11/Δ11p53+/−), display premature aging high frequency of spontaneous lymphoma mammary tumor formation. To investigate the role Brca1 regulation organ homeostasis susceptibility deficiency to environmental carcinogens, we examined...
Microtubules (MTs) are intracellular polymers that provide structure to the cell, serve as railways for transport, and regulate many cellular activities, including cell migration. The dynamicity function of MT cytoskeleton determined in large part by its regulatory proteins, recently discovered severing enzyme Fidgetin-like 2 (FL2). Downregulation FL2 expression with small interfering RNA (siRNA) results a more than twofold increase migration rate vitro well translates into improved...
Abstract Increased activity of the tumour suppressor p53 is incompatible with embryogenesis, but how controlled not fully understood. Differential requirements for inhibitors Mdm2 and Mdm4 during development suggest that these control mechanisms are context-dependent. Artery formation requires investment nascent endothelial tubes by smooth muscle cells (SMCs). Here, we find embryos lacking SMC β-catenin suffer impaired arterial maturation die E12.5, increased vascular wall activity....
Objective: Pediatric patients with autism spectrum disorder (ASD) often have coexisting feeding disorders. We hope to emphasize the significant implications that these disorders can on this patient population through a unique case of hypokalemia-induced rhabdomyolysis. Method: present 3-year-old boy ASD and longstanding history food selectivity whose routine was disrupted during COVID-19 pandemic resulting in avoidant/restrictive intake severe undernutrition, who presented profound...
In response to vascular injury, smooth muscle cells (SMCs) undergo phenotypic switching, with enhanced cell cycle entry and migration, loss of contractile protein expression. Previously, we found that the atypical cadherin Fat1 is upregulated in SMCs after injury. cultured SMCs, induced by growth factor stimulation, but limits SMC proliferation. Recently, species accumulate mitochondria interact critical proteins, including Complex I subunits. The factors governing significance mitochondrial...
Fat1 controls vascular smooth muscle cell (VSMC) growth and migration. In recent studies, we found that expression colocalizes with VSMCs in atherosclerotic lesions from apoE -/- mice, also identified the intermediate filament protein vimentin as a novel interactor. Like Fat1, is expressed affects growth. We hypothesized regulation of VSMC activities limits atherosclerosis, Fat1-vimentin interaction contributes to this regulation. To test idea, generated fat1 VSMC-KO ; double knockout (DKO)...
Molecular mechanisms that control the activities of vascular smooth muscle cells (VSMCs) in diseased or injured arterial wall remain incompletely understood. The atypical cadherin FAT1 is prominently expressed VSMCs after injury. In recent work, we found processing FAT1, a type I transmembrane protein, releases its intracellular domain, FAT1ICD; turn, FAT1ICD fragments accumulate mitochondria and interact with electron transport complexes II to restrict VSMC respiration cell growth...
The role of smooth muscle cell (SMC) mitochondria and metabolism in remodeling the systemic circulation is poorly understood. We have shown that FAT1 cadherin inhibits respiratory complex I (CI), respiration, SMC proliferation, opposes arterial occlusion after injury. hypothesize a ) limits key metabolic pathways for growth, b CI promotes activities relevant vascular remodeling. To study FAT1, we generated FAT1-deficient (KO) SMCs. These cells show enhanced growth associated to increased...