A5101722520- Circadian rhythm and melatonin
- Light effects on plants
- Genetics, Aging, and Longevity in Model Organisms
- Mitochondrial Function and Pathology
- Genetic Neurodegenerative Diseases
- Plant Molecular Biology Research
- Neuroscience of respiration and sleep
- Photoreceptor and optogenetics research
- Muscle Physiology and Disorders
- Neurobiology and Insect Physiology Research
- Epigenetics and DNA Methylation
- Adipose Tissue and Metabolism
- Heme Oxygenase-1 and Carbon Monoxide
- Spaceflight effects on biology
- Silk-based biomaterials and applications
- Photosynthetic Processes and Mechanisms
- Retinal Development and Disorders
- DNA Repair Mechanisms
- Medicinal Plant Research
- Amyotrophic Lateral Sclerosis Research
- Gout, Hyperuricemia, Uric Acid
- Reproductive tract infections research
- Virus-based gene therapy research
- Dietary Effects on Health
- Neonatal Health and Biochemistry
The University of Texas Health Science Center at Houston
2004-2016
National Taiwan University
2016
Baylor College of Medicine
1991-2004
Baylor Genetics
1992-2001
We show that, in the mouse, core mechanism for master circadian clock consists of interacting positive and negative transcription translation feedback loops. Analysis Clock/Clock mutant mice, homozygous Period2(Brdm1) mutants, Cryptochrome-deficient mice reveals substantially altered Bmal1 rhythms, consistent with a dominant role PERIOD2 regulation loop. In vitro analysis CRYPTOCHROME inhibition CLOCK: BMAL1-mediated shows that is through direct protein:protein interactions, independent...
Mammalian Per1 and Per2 genes are involved in the mechanism of circadian clock inducible by light. Alight pulse can evoke a change onset wheel-running activity mice shifting to earlier times (phase advance) or later delays) thereby advancing delaying (clock resetting). To assess role mouse Per ( mPer) resetting, carrying mutant mPer1 mPer2 were tested for responses light at ZT 14 22, respectively. The authors found that mutants did not advance delay clock. They conclude mammalian only...
Melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs, with five subtypes named M1–M5) are a unique subclass of RGCs axons that project directly to many brain nuclei involved in non-image-forming functions such as circadian photoentrainment and the pupillary light reflex. Recent evidence suggests melanopsin-based signals also influence image-forming visual function, including adaptation, but mechanisms unclear. Intriguingly, small population M1 ipRGCs have...
The expansion of polyglutamine tracts encoded by CAG trinucleotide repeats is a common mutational mechanism in inherited neurodegenerative diseases. Spinocerebellar ataxia type 6 (SCA6), an autosomal dominant, progressive disease, arises from repeat expansions present the coding region CACNA1A (chromosome 19p13). This gene encodes α<sub>1A</sub>, principal subunit P/Q-type Ca<sup>2+</sup> channels, which are abundant CNS, particularly cerebellar Purkinje and granule neurons. We assayed ion...
The mammalian period ( Per ) genes are components of the circadian clock and appear to be regulated via an autoregulatory feedback loop. Here we show that human PER1 hPER1 gene is synergistically activated by protein kinases A C (PKA, PKC) cAMP responsive element binding protein. Activators inhibitors PKA as well PKC modulate endogenous expression promoter‐driven reporter activity in a dose‐dependent manner. Our results suggest promoter acts sensor for multiple signaling molecules thereby...
Biochemical and mechanistic aspects into how various hypometabolic states are initiated in mammals poorly understood. Here, we show a state of hypometabolism is by 5′-AMP uptake erythrocytes. Wild type, ecto-5′-nucleotidase-deficient, adenosine receptor-deficient mice undergo 5′-AMP-induced similar fashion. Injection leads to two distinct declining phases oxygen consumption (VO2). The phase I response displays rapid steep decline VO2 that independent body temperature (Tb) ambient (Ta). It...
We report the restoration of 430-kD dystrophin in mdx, mouse model Duchenne muscular dystrophy, by expression a single-copy recombinant transgene. Muscle-specific was achieved using creatine kinase promoter influenced two enhancers. Immunostaining with anti-Xp21-coded monoclonal antibodies showed that localized to muscle fiber membrane. However, there variability level various animals aging, between fast and slow muscles, within different regions same muscle. Curiously, relatively absent...