Publications by authors named "Athuluri Divakar Sai Krishna"

TACI signals activate B cell proliferation, isotype switch and antibody production in both normal immunity and autoimmune states. In contrast to murine TACI, the human TACI gene undergoes alternative splicing to produce short and long isoforms (TACI-S and TACI-L). In previous studies, we showed that transduction of the short, but not long isoform, into murine B cells or human pre-B cells lacking TACI, caused them to become transcriptional and morphologically identical to plasma cells.

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Chronic fibrotic liver disease caused by viral or metabolic etiologies is a high-risk condition for developing hepatocellular carcinoma (HCC). Even after curative treatment of early-stage HCC tumor, the carcinogenic microenvironment persists in the remnant diseased liver and supports the development of de novo HCC tumors (de novo HCC recurrence). Therefore, prevention of HCC development in patients at risk of not only first-primary but also second-primary HCC tumors is theoretically the most impactful strategy to improve patient prognosis.

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Article Synopsis
  • - Activating mutations in RAS genes are responsible for 20%-30% of human cancers, making RAS inhibitors a crucial area of cancer research, but developing them has been difficult.
  • - Researchers have discovered that rigosertib, a specific compound, can mimic RAS and prevent RAF kinases from interacting with RAS, thereby disrupting a key cancer signaling pathway.
  • - Rigosertib also binds to other proteins involved in RAS signaling, suggesting a broader potential to inhibit RAS pathways in various cancers through targeting common interaction domains.
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Background: Cancerous state is a highly stimulated environment of metabolically active cells. The cells under these conditions over express selective receptors for assimilation of factors essential for growth and transformation. Such receptors would serve as potential targets for the specific ligand mediated transport of pharmaceutically active molecules.

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