Educational Forum with Clinical Studies Current Science and Research

June 17, 2011

Selective Loss of Sertoli Cell and Germ Cell Function Leads to a Disruption in Sertoli Cell-Germ Cell Communication During Aging in the Brown Norway Rat. Xanya Sofra Weiss

Filed under: Xanya Sofra Weiss — Tags: — Dr. Xanya @ 6:19 am

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We investigated the effects of aging on Sertoli cell-germ cell interactions from Brown Norway rats using the induction of four specific mRNAs as markers. The testes from aging (24 mo old) Brown Norway rats can be normal size or regressed. One marker, a von Ebner’s-like protein, is expressed in coculture and “in vivo” in germ cells from normal testes of 6- and 24-mo-old rats but not in germ cells from regressed testes of 24-mo-old rats. A second germ cell marker, the Huntington disease protein, is expressed in all germ cells. Two Sertoli cell markers, a serotonin receptor and a novel gene, are induced in Sertoli cells by meiotic germ cells. The serotonin receptor mRNA is expressed in Sertoli cells from 20-day, 6-mo, and 24-mo normal testes but not in those from 24-mo regressed testes. The novel gene is induced in Sertoli cells from all testes. We conclude that Sertoli cells from aged regressed testes are unable to respond to selective signals from germ cells from young rats, and germ cells from regressed testes show a similar selective loss. Such disruptions in communication between Sertoli cells and germ cells likely contribute to germ cell loss during aging.

Xanya Sofra Weiss

Xanya Sofra Weiss

Abl Protein-Tyrosine Kinase Inhibitor STI571 Inhibits In Vitro Signal Transduction Mediated by c-Kit and Platelet-Derived Growth Factor Receptors. Xanya Sofra Weiss

Filed under: Xanya Sofra Weiss — Tags: — Dr. Xanya @ 6:17 am

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STI571 (formerly known as CGP 57148B) is a protein-tyrosine kinase inhibitor that is currently in clinical trials for the treatment of chronic myelogenous leukemia. STI571 selectively inhibits the Abl and platelet-derived growth factor (PDGF) receptor tyrosine kinases in vitro and blocks cellular proliferation and tumor growth of Bcr-abl– or v-abl-expressing cells. We have further investigated the profile of STI571 against related recep- tor tyrosine kinases. STI571 was found to potently inhibit the kinase activity of the

Global landscape of protein complexes in the yeast Saccharomyces cerevisiae. Xanya Sofra Weiss

Filed under: Xanya Sofra Weiss — Tags: — Dr. Xanya @ 6:15 am

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Identification of protein–protein interactions often provides insight into protein function, and many cellular processes are performed by stable protein complexes. We used tandem affinity purification to process 4,562 different tagged proteins of the yeast Saccharomyces cerevisiae. Each preparation was analysed by both matrix-assisted laser desorption/ ionization–time of flight mass spectrometry and liquid chromatography tandem mass spectrometry to increase coverage and accuracy. Machine learning was used to integrate the mass spectrometry scores and assign probabilities to the protein–protein interactions. Among 4,087 different proteins identified with high confidence by mass spectrometry from 2,357 successful purifications, our core data set (median precision of 0.69) comprises 7,123 protein–protein interactions involving 2,708 proteins. A Markov clustering algorithm organized these interactions into 547 protein complexes averaging 4.9 subunits per complex, about half of them absent from the MIPS database, as well as 429 additional interactions between pairs of complexes. The data (all of which are available online) will help future studies on individual proteins as well as functional genomics and systems biology.

Xanya Sofra Weiss

Xanya Sofra Weiss

June 10, 2011

Protein turnover plays a key role in aging. Xanya Sofra Weiss

Filed under: Xanya Sofra Weiss — Tags: — Dr. Xanya @ 3:46 am

Although the molecular mechanism of aging is unknown, a progressive increase with age in the concentration of damaged macromolecules,

especially proteins, is likely to play a central role in senescent decline. In this paper, we discuss evidence that the progressive decrease in protein

synthesis and turnover can be the primary cause of the increase in the concentration of damaged proteins with age. Conversely, protein damage itself

is likely to be the cause of the decrease in protein turnover. This could establish a positive feedback loop where the increase in protein damage decreases

the protein turnover rate, leading to a further increase in the concentration of damaged proteins. The establishment of such a feedback loop should result in

an exponential increase in the amount of protein damage—a protein damage catastrophe—that could be the basis of the general deterioration observed in senescent organisms.

© 2002 Published by Elsevier Science Ireland Ltd.

Xanya Sofra Weiss

Xanya Sofra Weiss

Parasympathetic nerve-evoked protein synthesis, mitotic activity and salivary secretion in the rat parotid gland and the dependence on NO-generation. Xanya Sofra Weiss

Filed under: Xanya Sofra Weiss — Tags: — Dr. Xanya @ 3:44 am

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Incorporation of radiolabelled leucine and thymidine into trichloroacetic acid-insoluble material of the parotid gland was used as indices of protein synthesis and mitotic activity, respectively, following electrical stimulation of the parasympathetic auriculo-temporal nerve for 30 min in pentobarbitone-anaesthetized rats under adrenoceptor blockade (phentolamine and propranolol, 2 mg/kg intravenous of each) in the absence or presence of atropine (2 mg/kg intravenous) and without or with nitric oxide synthase inhibitors. In atropinized rats, the parasympathetic non-adrenergic, non-cholinergic (NANC) nerve-evoked mean increases in protein synthesis at a frequency of 10 Hz (142%) and 40 Hz (200%) were not affected in a statistically significant way (124 and 275%, respectively) by the neuronal type NO-synthase inhibitor Nwpropyl-L-arginine (N-PLA) (30 mg/kg intravenous). Neither were the increase (175%) in protein synthesis at 10 Hz in non-atropinized animals affected by N-PLA (180%). The increase (65%) in mitotic activity, 19 h after the end of stimulation at 40 Hz, in the presence of atropine, was not affected by N-PLA (55%). Neither were the increase (95%) in gland content of amylase at this point of observation statistically significant affected by N-PLA (144%). The secretion of fluid and output of amylase from the parotid gland upon nerve stimulation was not affected by N-PLA. When examining the non-selective NO-synthase inhibitor L-NAME (30 mg/kg intravenous) in atropinized rats subjected to stimulation at 10 Hz, neither the increase in protein synthesis nor the evoked fluid response or amylase outputs were affected. Hence, in contrast to an NO-dependent sympathetic-induced protein synthesis and mitosis in the parotid gland, involving the activity of the neuronal type NO-synthase, no support for a parasympathetic-induced protein synthesis (and gain in gland amylase) and mitosis, depending on NO-generation, was found.

Xanya Sofra Weiss

Xanya Sofra Weiss

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