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S Shenoy

Publications and source records attributed to S Shenoy.

12 recordsLinked to original sources
PubMed1992

Role of p34cdc2-mediated phosphorylations in two-step activation of pp60c-src during mitosis.

Phosphorylation of pp60c-src by p34cdc2 at three amino-proximal serine/threonine residues is temporally correlated with, but insufficient for, mitotic activation of c-Src kinase. The direct cause of activation during mitosis appears to be temporally correlated partial dephosphorylation of Tyr-527, a residue whose phosphorylation strongly suppresses pp60c-src activity. Site-directed mutagenesis of the serine/threonine phosphorylation sites blocks half the mitosis-specific decrease in Tyr-527 phosphorylation and half the increase in pp60c-src kinase activity. We conclude that p34cdc2 partially activates pp60c-src by a two-step process in which its serine/threonine phosphorylations either sensitize pp60c-src to a Tyr-527 phosphatase or desensitize it to a Tyr-527 kinase. Furthermore, additional events, independent of these p34cdc2-mediated phosphorylations, participate in mitotic activation of pp60c-src.

3T3 Cells↗
PubMed1992

c-Src and mitosis.

The transforming potential and by inference the physiological function of the proto-oncoprotein pp60c-src closely correlate with the level of its protein tyrosine kinase activity. We have investigated the cell cycle-dependent regulation of this activity using mouse fibroblasts overexpressing chicken or mouse pp60c-src as a model system. During mitosis pp60c-src becomes phosphorylated at specific serine and threonine residues by p34cdc2. At the same time its tyrosine kinase activity, assayed in vitro, is increased approximately twofold and accessibility of its SH2 domain for binding relevant phosphotyrosine-containing ligands increases by about 15-fold. A kinase-defective mutant of pp60c-src exhibits a substantial (50-70%) decrease in phosphorylation at Tyr527 during mitosis. Phosphorylation of this residue negatively regulates kinase activity. Indirect evidence indicates a lesser decrease in wild-type pp60c-src Tyr527 phosphorylation during mitosis. Coordinate mutation of the mitosis-specific phosphorylation (MSP) sites in kinase-defective pp60c-src greatly reduces, though does not abolish, its mitosis-specific tyrosine dephosphorylation. Similarly, coordinate mutation of the three MSP sites in chicken pp60c-src or the corresponding two sites in mouse pp60c-src does not completely block mitotic stimulation of kinase activity. Thus, additional events beyond p34cdc2-mediated phosphorylation are involved in cell-cycle dependent regulation of pp60c-src activity. This is also suggested by the stimulation of pp60c-src kinase activity and decrease in phosphorylation of Tyr527 observed following treatment of fibroblasts with okadaic acid, a potent inhibitor of types 1 and 2A serine/threonine phosphatases. The potential role of cell cycle-dependent regulation of phosphatases and kinases acting on the regulatory tyrosine residue of pp60c-src is discussed.

Animals↗
PubMed1990

Pediatric cancer care in India. A national survey.

A national survey of institutions treating children with cancer was undertaken in April 1988. The 21-item questionnaire included questions on personnel, treatment facilities, support services, attitudes and opinions regarding pediatric cancer care. 73 institutions responded. From the survey, it emerged that pediatricians did not see all pediatric patients with cancer at one-third of the respondent institutions. 50 percent of cancer centres did not have pediatricians. Cancer centres were better staffed with specialist personnel and better support services. Respondents felt that pediatric oncologists and specialist support personnel were necessary for optimal pediatric cancer care and facilities at medical colleges needed to be improved because of the large number of children with cancer treated at these institutions.

Child↗
PubMed1989

Purified maturation promoting factor phosphorylates pp60c-src at the sites phosphorylated during fibroblast mitosis.

We have previously shown that overexpressed chicken pp60c-src has retarded mobility, novel serine/threonine phosphorylation, and enhanced kinase activity during NIH 3T3 cell mitosis. Here we show that novel mitotic phosphorylations occur at Thr 34, Thr 46, and Ser 72. The possibility, previously raised, that Ser 17 is dephosphorylated during mitosis is excluded. The phosphorylated sites lie in consensus sequences for phosphorylation by p34cdc2, the catalytic component of maturation promoting factor (MPF). Furthermore, highly purified MPF from metaphase-arrested Xenopus eggs phosphorylated both wild-type and kinase-defective pp60c-src at these sites. Altered phosphorylation alone is sufficient to account for the large retardation in mitotic pp60c-src electrophoretic mobility: phosphorylation of normal pp60c-src by MPF retarded mobility and dephosphorylation of mitotic pp60c-src restored normal mobility. These results suggest that pp60c-src is one of the targets for MPF action, which may account in part for the pleiotropic changes in protein phosphorylation and cellular architecture that occur during mitosis.

Amino Acid Sequence↗
PubMed1979

Light and ultrastructural studies of renal oncocytic adenoma.

An asymptomatic renal oncocytoma was found in the upper left quadrant of an eighty-five-year-old woman during a routine physical examination. Ultrastructurally, the tumor was composed entirely of epithelial cells filled with normal and abnormal mitochondria. Selective renal angiography showed two renal arteries supplying a lobulated, highly vascular mass. The mass contained irregular and tortuous vessels without any arteriovenous shunting.

Adenoma↗
PubMedDate not supplied

Arteriovenous malformation of the cecum: report of six cases.

Patients who have chronic lower gastrointestinal bleeding with negative conventional work-ups should undergo superior mesenteric arteriography to look for arteriovenous malformations. Once the diagnosis is made, treatment is immediate conventional right hemicolectomy. Six patients with arteriovenous malformations described in this report have had no recurrence of rectal bleeding in one to five years.

Adult↗
PubMedDate not supplied

Transmission of enteric non-A, non-B hepatitis virus in Macaca mulatta monkeys by intraportal route: subsequent passages of HEV virus.

Macaca mulatta monkeys have been used for the transmission of enteric non-A, non-B hepatitis (HEV) virus by intraportal route. Subsequent passages of HEV virus have been completed in these monkeys. In the first passage, 2 monkeys were inoculated by intra-portal route with 27-34 nm virus-like particles (VLP) obtained from known epidemics of HEV hepatitis in India, and biochemical and serological changes in the blood, histological changes in the liver and excretion of 27-34 nm VLP in the stool were studied. Results were compared with those of 4 negative control monkeys inoculated with stool extracts from healthy individuals. The second passage of 27-34 nm VLP was carried out on 2 monkeys using pools of stool suspension positive for 27-34 nm VLP from first passaged animals. Similarly, the third passage of 27-34 nm VLP was completed intraportally in another monkey. All monkeys developed acute hepatitis, as evidenced by transient elevation of aminotransferase, histopathological changes in the liver, development of antibodies aggregating 27-34 nm VLP and excretion of 27-34 nm VLP in stools. No control monkeys developed these features.

Animals↗