Biomedical subjects

N Divecha

Publications and source records attributed to N Divecha.

39 records · Page 3Linked to original sources

PubMed1991

The polyphosphoinositide cycle exists in the nuclei of Swiss 3T3 cells under the control of a receptor (for IGF-I) in the plasma membrane, and stimulation of the cycle increases nuclear diacylglycerol and apparently induces translocation of protein kinase C to the nucleus.

When Swiss 3T3 cells are treated with Insulin-like Growth Factor I, a rapid decrease in the mass of polyphosphoinositol lipids (phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate) occurs within the nuclei, with a concomitant increase in nuclear diacylglycerol and translocation of protein kinase C to the nuclear region. This is in contrast to the effects of the regulatory peptide, bombesin, which causes similar inositol lipid changes in the plasma membrane, has no effect on nuclear inositide levels and causes a translocation of protein kinase C to post-nuclear membranes. These results suggest the existence of a discrete nuclear polyphosphoinositide signalling system entirely distinct from the well-known plasma membrane-located system, which is under regulatory control by cell surface-located receptors.

3T3 Cells↗

PubMed1989

Basic proline-rich proteins of murine parotid glands. Induction of mRNA by isoprenaline and post-secretion processing.

Five major basic polypeptides with characteristics typical of proline-rich proteins, accumulated in parotid glands after long term isoprenaline treatment of Balb C mice. They were studied by two-dimensional gel electrophoresis and designated B1 degree, B2' degrees, B2 degrees, B3 degrees and B4 degrees on the basis of pI-dependent mobility. They were not observed in the glands of normal mice and were precipitated when glands were homogenized in 10% trichloroacetic acid unlike the three isoprenaline-induced proline-rich proteins of murine parotid glands reported previously. Isoprenaline induced six proline-rich in vitro translation products which were absent normally. Four of these species had pI-dependent mobilities almost identical to B1 degree, B2 degrees, B3 degrees and B4 degrees, indicating not only precursor/product relationships, but also that isoprenaline induced the accumulation of the proteins by regulating the mRNA. Identical salivary counterparts of the basic glandular proline-rich proteins were not detected whereas a series of smaller and more basic isoprenaline-induced polypeptides were observed in saliva (major speices B1s-B4s). The glandular proline-rich proteins were secreted from parotid tissue in vitro and the data indicate that proline-rich proteins are synthesised as precursors and processed into salivary form in the parotid glands after secretion. The relationships between the B-type in vitro translation products, parotid gland precursors and salivary proteins were also confirmed immunologically.

Animals↗

PubMed1989

Isoprenaline-induced and constitutive members of a proline-rich protein sub-group from mouse parotid glands studied with monoclonal antibody NAL1.

Members of the proline-rich protein (PRP) family of mouse parotid glands were analysed before and after stimulation with the beta-agonist isoprenaline by using a monoclonal antibody raised against the induced PRP A3(0) (GP-27). Antibody NAL1 reacted strongly with isoprenaline-induced B-type PRP precursors and their salivary counterparts, but not against the A-type PRPs A1(0) (Gp-66) and A2(0) (GP-45) or human salivary proteins, and it is likely that NAL1 recognizes a proline-rich repeat variant unique to this group of rodent PRPs. PRP-related antigens were observed in the parotid glands (N1(0) and N2(0] and saliva of normal mice. The antigens were located immunocytochemically in secretory granules of parotid acinar cells of both normal and isoprenaline-stimulated mice. The total amount of PRP antigens increased 16-fold from 2.5 to 40% of parotid protein after 10 days of isoprenaline treatment, as estimated by enzyme-linked immunosorbent assay. Immunoblotting showed that new PRP species appeared during the period of increase. After treatment with isoprenaline, B-type PRPs appeared first, followed by A3(0) and another member of the family. These results show that the mouse PRP family is larger than previously thought and can be divided immunologically into sub-groups. That a subset of PRPs are produced in the normal mouse indicates that there is differential beta-adrenergic regulation within the family, and also has implications for the role of PRPs in the normal maintenance of healthy dentition and other processes.

Animals↗