A5072335818- Mitochondrial Function and Pathology
- ATP Synthase and ATPases Research
- Inflammasome and immune disorders
- Metabolism and Genetic Disorders
- RNA Interference and Gene Delivery
- RNA modifications and cancer
- RNA and protein synthesis mechanisms
- Cytomegalovirus and herpesvirus research
- Redox biology and oxidative stress
- Cell death mechanisms and regulation
- Erythrocyte Function and Pathophysiology
- Trace Elements in Health
- Advanced Nanomaterials in Catalysis
- Metalloenzymes and iron-sulfur proteins
- Infectious Encephalopathies and Encephalitis
Texas A&M University
2019-2024
Salk Institute for Biological Studies
2024
Significance The assembly and function of membrane proteins depend on the lipid milieu. In recent years protein components mitochondrial calcium uniporter have been identified, but its specific phospholipid requirements are not known. Utilizing yeast mutants defective in their ability to synthesize different phospholipids, we identify a requirement cardiolipin (CL) stability uniporter. Our findings translatable higher organisms because endogenous abundance is decreased patient-derived cells...
Iodine (I2) is an extremely popular reagent for disulfide assembly in solution, solid phase (pseudo‐dilute conditions) peptides, and immobilized materials. However, we noticed that I2‐mediated peptide often resulted incomplete reactions due to its redox activity under pseudo‐dilute conditions. The phenomenon intrigued us conduct in‐depth analysis of with various sequences. We revealed the equilibrium between free thiols products was sequence‐dependent previously unsolicited. Adding TEMPO...
Abstract Calcium signaling via mitochondrial calcium uniporter (MCU) complex coordinates bioenergetics with cellular energy demands. Emerging studies show that the stability and activity of pore-forming subunit complex, MCU, is dependent on phospholipid, cardiolipin (CL), but how this impacts calcium-dependent in CL-deficiency disorder like Barth syndrome (BTHS) not known. Here we utilized multiple models BTHS including yeast, mouse muscle cell line, as well patient cells cardiac tissue to...
Signaling circuits crucial to systemic physiology are widespread, yet uncovering their molecular underpinnings remains a barrier understanding the etiology of many metabolic disorders. Here, we identified copper-linked signaling circuit activated by disruption mitochondrial function in murine liver or heart that resulted atrophy spleen and thymus caused peripheral white blood cell deficiency. We demonstrated leukopenia was α-fetoprotein, which required copper surface receptor CCR5 promote...
Abstract Signaling circuits crucial to systemic physiology are widespread, yet uncovering their molecular underpinnings remains a barrier understanding the etiology of many metabolic disorders. Here, we identify copper-linked signaling circuit activated by disruption mitochondrial function in murine liver or heart that results atrophy spleen and thymus causes peripheral white blood cell deficiency. We demonstrate leukopenia is caused α-fetoprotein, which requires copper surface receptor CCR5...