Biomedical subjects

C Sudhakar

Publications and source records attributed to C Sudhakar.

7 recordsLinked to original sources

PubMed1999

Induction of p53 dependent apoptosis upon overexpression of a nuclear protein tyrosine phosphatase.

Two ubiquitously expressed protein tyrosine phosphatases, PTP-S2 and PTP-S4 (also known as TC45 and TC48, respectively), are alternately spliced products of the same gene. Overexpression of PTP-S2 by transient transfection induced chromatin condensation and nuclear fragmentation, typical of apoptosis. Expression of PTP-S4 resulted in a much lower number of cells with apoptotic phenotype. PTP-S2 induced apoptosis in MCF7 and A549 human tumor cell lines which are p53 positive but not in HeLa and SW620 cells which are p53 negative. Apoptosis induced by PTP-S2 in MCF7 cells was inhibited by cotransfection with mutant p53 (Arg-273 --> His) but not by wild type p53. PTP-S2 induced apoptosis was inhibited by antiapoptotic protein Bcl2 and certain inhibitors of caspases. These results suggest that the nuclear tyrosine phosphatase PTP-S2 induces p53 dependent, serum starvation independent and caspase mediated apoptosis.

Animals↗

PubMed1998

Exomphalos.

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Consanguinity↗

PubMed1997

Response of some Calvin cycle enzymes subjected to salinity shock in vitro.

Leaf enzyme extracts of 10 day old seedlings of horsegram were subjected to NaCl or Na2SO4 treatment in vitro. Salinity shock caused decline in the activities of RuBP carboxylase, R-5-P kinase, R-5-P isomerase and NADP-Gly-3-P dehydrogenase. At low concentrations, Na2SO4 did not alter the activities of R-5-P kinase, R-5-P isomerase and NADP-Gly-3-P dehydrogenase. RuBP carboxylase was found to be more sensitive to salt shock than the other enzymes studied. Further, NaCl was more toxic to the enzyme activities as compared to Na2SO4.

Osmotic Pressure↗

PubMed1995

Cell free ascitic fluid prevents loss of cell surface sialic acid from Zajdela Ascitic Hepatoma cells in culture.

In the Zajdela Ascitic Hepatoma (ZAH), a rat tumor, high levels of cell surface sialic acid residues are present which masked the immunogenicity of the cells. We have shown here that cell surface sialic acid level goes down rapidly when ZAH cells are put in culture. The reduction in surface sialic acid levels is due to a decrease in sialic acid residues on the major sialylated glycoprotein, gp 120, as well as a decrease in gp 120 polypeptide. The loss of sialic acid from the cultured cells is reduced if the cells are cultured in the presence of cell free ascitic fluid from ZAH tumor.

Animals↗

PubMed1993

Regulation of expression of beta-galactoside alpha 2,6-sialyltransferase in a rat tumor, Zajdela ascitic hepatoma.

Tumor cell surface sialic acid levels determine a number of important properties governing cellular interactions and cell-cell communication. Towards understanding the mechanism of regulation of sialic acid levels upon cellular transformation, we have studied the regulation of expression of beta-galactoside alpha 2,6-sialyltransferase in a rat tumor, the Zajdela ascitic hepatoma. We demonstrate distinct differences in the regulation of expression of the enzyme in the tumor cells as compared to normal liver cells. The expression of sialyltransferase is regulated both at the transcriptional and post-transcriptional level in a tissue-specific manner.

Animals↗

PubMed1993

Differential expression of thymidine kinase gene in two subpopulations of a rat tumour correlates with their tumorigenic and cell division potential.

We have studied the expression of the thymidine kinase (TK) gene in two kinetically heterogenous populations of a rat tumour cell line--the Zajdela ascitic hepatoma (ZAH). We have demonstrated that the TK gene is differentially expressed in the two cell types. The more tumorigenic and rapidly dividing subpopulation shows higher levels of mRNA and enzyme activity for TK. In addition, we have shown that the tumorigenic cells accumulate the primary unspliced transcript and utilise only part of it for maturation. It is, therefore, likely that ZAH cells regulate their division and possibly tumorigenic potential by regulating the expression of the TK gene.

Animals↗

PubMed1990

Differential amplification and expression of c-myb oncogene in Zajdela ascitic hepatoma.

Organisation and expression of c-myb protooncogene have been studied in a heterogeneous tumour the Zajdela ascitic hepatoma (ZAH). The myb gene is selectively amplified in the more tumorigenic subpopulation of the tumour while the non-lethal subpopulation does not show any change. Analysis of transcripts of the myb gene in tumorigenic versus nontumorigenic cells shows that the level of amplification of the gene does not correspond to the level of its transcription. Results have been discussed in the light of existing evidence regarding the role of c-myb gene expression during cell cycle.

Animals↗