Example sentences for: adp-ribosylation

How can you use “adp-ribosylation” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • ADP-ribosylation of Rho proteins by C3 exoenzyme prevents neurite retraction in the specialized growth cone of developing neurons, and in fact promotes neurite outgrowth in the same fashion as microinjection of purified dominant negative RhoA T19N [ 39 ] . In these instances, neuronal N1E-115 cell outgrowth induced by inactivation of RhoA was mimicked by microinjection of Rac1- or Cdc42-GST fusion proteins, and could be abolished by coinjection of dominant negative Cdc42 T17Nor Rac1 T17N [ 39 ] . From these results, the authors concluded that inactivation of RhoA by C3 exoenzyme treatment resulted in the activation of Rac1 and Cdc42 GTPases, suggesting the mutually exclusive function of RhoA and Rac1/Cdc42.

  • ADP-ribosylation of Rho proteins in chemoattractant stimulated neutrophils [ 20 21 ] and in both monocytic lines and fresh blood monocytes [ 22 38 ] results in actin filament polymerization.

  • Similar observations were obtained for other gene clusters, including amylases on 1p21, annexins on 4q21, homeobox proteins on 7p15 and 17q21, metallothioneins on 16q13, crystalline proteins on 2q33, glutathione- S -transferases (m1, m2, m3, m4 and m5) on 1p13, histone families (H2A/H2B/H3/H4) on 6p21, killer cell lectin-like receptors on 12p13, proline-rich proteins on 12p13, protocadherins on 5p15, s100 calcium-binding proteins on 1q21, keratins on 17q12, ADP-ribosylation factors (3, 4 and 5) on 10q22, and the major histocompatibility complex on 6p21.

  • The involvement of Rho GTPases in regulating integrin dependent events such as leukocyte homotypic aggregation and in chemokine upregulation of integrin-mediated adhesion has recently been identified [ 18 19 ] . ADP-ribosylation of Rho in neutrophils by treatment with C3 not only inhibits cellular locomotion, but augments chemoattractant induced actin polymerization [ 20 21 ] . Moreover, inactivation of Rho in monocytic cells leads to accelerated formation of filopodia, and it has been proposed that Rho is a negative regulator of actin polymerization within this cell type [ 22 ] . Active Rho is also required for normal morphology, motility, and cytolytic activity of IL-2 activated NK cells [ 23 24 ] . We and others have demonstrated the importance of Rho in T lymphocyte activation [ 25 26 ] . Given the role played by Rho in the regulation of actin microfilaments in other cell types, and the indispensability of a functional actin cytoskeleton in lymphocyte motility and activation, it is of importance to study Rho's role in the regulation of T lymphocyte integrin function and maintenance of cytoskeletal organization.

  • Previous reports have demonstrated that ADP-ribosylation of B-lymphoid cell lines by C3 treatment inhibits phorbol ester induced cellular homotypic aggregation [ 18 ] . Also, phorbol ester and chemoattractant (IL-8 and fMLP) induced pre-B lymphoblastoid adhesion to VCAM-1 and neutrophil adhesion to fibrinogen was abrogated in a dose-dependent manner by C3 exoenzyme [ 36 ] . This may indicate that in cells of hematopoietic lineages, the induction of an increased adhesive state may be susceptible to regulation by Rho proteins.


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