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[
Worm Breeder's Gazette,
1994]
Cytology of degenerin-induced cell death in the PVM neuron David H. Hall, Guoqiang Gu+, Lei Gong#, Monica Driscoll#, and Martin Chalfie+, * Dept. Neuroscience, Albert Einstein College of Medicine, Bronx, N.Y. 10461 + Dept. Biological Sciences, Columbia University, New York, N.Y. 10027 # Dept. Molecular Biology and Biochemistry, Rutgers University, Piscataway, N.J. 08855
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[
Worm Breeder's Gazette,
1994]
More degenerins in the worm? Harbinder Singh Dhillon and Monica Driscoll. Department of Molecular Biology and Biochemistry, Rutgers University, Center for Advanced Biotechnology and Medicine, 679 Hoes lane, Piscataway, N.J. 08855
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[
Worm Breeder's Gazette,
1994]
THE MATERNAL GENE SKN-4 AND THE SPECIFICATION OF VENTRAL BLASTOMERE FATES IN THE EARLY C. ELEGANS EMBRYO Bruce Bowerman, Paula R. Martin, Christopher J. Thorpe, and Christopher A. Shelton. The Institute of Molecular Biology, University of Oregon, Eugene, OR 97403.
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[
Chem Soc Rev,
2009]
On December 10, 2008 Osamu Shimomura, Martin Chalfie and Roger Tsien were awarded the Nobel Prize in Chemistry for "the discovery and development of the green fluorescent protein, GFP". The path taken by this jellyfish protein to become one of the most useful tools in modern science and medicine is described. Osamu Shimomura painstakingly isolated GFP from hundreds of thousands of jellyfish, characterized the chromophore and elucidated the mechanism of Aequorean bioluminescence. Martin Chalfie expressed the protein in E. coli and C. elegans, and Roger Tsien developed a palette of fluorescent proteins that could be used in a myriad of applications.
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[
International Worm Meeting,
2021]
Neurodegenerative diseases such as Alzheimer's disease (AD) are well recognized as major public health problems in the aged population. Recognized events in AD include cognitive impairment, oxidative stress (OS), AB plaques accumulation in brain tissue. The current drugs to treat AD no cure or reduce the progression of the disease. Thus, the study of different extracts can provide a wealth of bioactive compounds and their combination, which can exert a new strategy for several neurodegenerative diseases, including AD. Among the natural extracts, Ginkgo biloba is one of the most investigated herbal remedies for cognitive disorders and AD. Moreover, docosahexaenoic acid (DHA), and Pinitol and Ursolic acid (UA) are associated to a prophylactic role in certain age-related diseases with particular emphasis on some of the effects of certain degenerative diseases. This study aimed to investigate the synergistic neuroprotective effects of mixed extract composed by different concentrations of DHA (150 microM), Ginkgo (120 microM) Pinitol (105 microM), and UA (35 microM) from Biosearch Life product, including OS tolerance, Thioflavin-S staining AB plaques, and lifespan in several transgenic Caenorhabditis elegans (C. elegans) as well as cognitive performance in C. elegans and senescence-accelerated prone mice 8 (SAMP8) model. Firstly, we found a significantly higher survival percentage in C. elegans treated with Mix extract group in comparison with the single extract treated groups (DHA 150 microM group, Ginkgo 120 microM group, Pinitol 105 microM group, UA 35 microM group), reaching the Vitamin C group. Likewise, we found a significantly increased the lifespan in C. elegans Mix extract-treated group compared to the other groups, suggesting the synergistic effects. Remarkably, we determined a significant reduction in AB plaques accumulation in C. elegans strain CL2006 Mix extract group compared to other groups, including all treated groups, confirming the synergistic effect again. Finally, we demonstrated better cognitive performance in the Mix extract group in both AD models (neuronal AB C. elegans strain CL2355 and SAMP8 mice model), confirming the molecular result and demonstrating the synergist effects of this Mix extract. Taken together, our results demonstrated the potential therapeutic strategy for AD of this new Mix extract product from Biosearch Life.
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[
Worm Breeder's Gazette,
1992]
A Hot-spot for Mutations in a Cys-rich Domain of
mec-4 Includes a Site Which, When Mutated, Can Suppregg a Dominant Death inducing Mutation in Cis Kyonsoo Hong and Monica Driscoll. Department of Molecular Biology and Biochemistry, Rutgers University, Center for Advanced Biotechnology and Medicine, 679 Hoes Lane, Piscataway, N.J. 08855 (908) 463-5193
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[
Worm Breeder's Gazette,
1990]
In the previous issue of the WBG (Vol. 11, #3, page 20) we reported the isolation of a cysteine protease clone from a mixed-stage C. elegans cDNA library. This library was originally obtained from Chris Martin and not from Cynthia Kenyon as was reported in the article. Our apologies for any misunderstanding caused by this oversight.
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[
Journal of Gerontology,
1999]
In recent years, oxidative damage to macromolecules has gained popularity as the basis of the molecular mechanism of aging. Martin proposes oxidative damage to macromolecules as one of the major public mechanisms of aging. Interest in modifications of protein by reactive oxygen species in aging was apparently introduced by Stadtman. Although various types of oxidative modifications can occur in proteins, carbonyl residues believed to be generated by metal catalyzed reaction or otherwise introduced by lysine, arginine and/or proline residues in vivo are often used as a marker of direct or
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[
Cell,
2004]
Heterotrimeric G proteins are well known for their function in signal transduction downstream of seven transmembrane receptors. More recently, however, genetic analysis in C. elegans and in Drosophila has revealed a second, essential function of these molecules in positioning the mitotic spindle and attaching microtubules to the cell cortex. Five new publications in Cell (Afshar et al., 2004; Du and Macara, 2004 [this issue of Cell]; Hess et al., 2004), Developmental Cell (Martin-McCaffrey et al., 2004), and Current Biology (Couwenbergs et al., 2004) show that this function is conserved in vertebrates and-like the classical pathway- involves cycling of G proteins between GDP and GTP bound conformations.
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[
Mol Biol Cell,
2008]
Monitoring Editor: Tom U. Martin The anti-epileptic valproate (VPA) is widely used in the treatment of bipolar disorder, although the mechanism of its action in the disorder is unclear. We show here that VPA inhibits both inositol phosphate and diacylglycerol (DAG) signaling in C.elegans. VPA disrupts two behaviors regulated by the inositol 1,4,5-Tris phosphate (IP3): defecation and ovulation. VPA also inhibits two activities regulated by DAG signaling: acetylcholine (ACh) release and egg-laying. The effects of VPA on DAG signaling are relieved by phorbol ester, a DAG analog, suggesting that VPA acts to inhibit DAG production. VPA reduces levels of DAG and IP1, but PIP2 is slightly increased, suggesting that Phospholipase C mediated hydrolysis of PIP2 to form DAG and IP3 is defective in the presence of VPA.