Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possibility that the mitogenic effect of fibrinogen, a major plasma protein (3 mg/ml), is mediated by specific membrane receptors was studied. Specific binding analysis showed that fibrinogen receptors are present only on hemopoietic cell lines that respond to its mitogenic effect. The mitogenic fibrinogen receptor is not recognized by antibodies specific for the platelet fibrinogen receptor or is not competitively blocked by synthetic peptides containing the Arg-Gly-Asp sequence, which is common to fibronectin, fibrinogen, vitronectin, and other cell-attachment proteins. The lymphoma-derived pre-B-cells (Raji) have 149,000 receptors, whereas the lymphoma-derived T cells (JM), which are 3 times smaller, have 54,000 receptors. These receptors have a Kd of 2 X 10(-7) M. They are inducible by stimuli specific for the cell lineage: activators of the breakdown of phosphatidylinositol phosphates, such as platelet activating factor for Raji cells, and adenylate cyclase agonists and cAMP analogues for JM cells. The stimuli have no mitogenic effect in the absence of fibrinogen; they do not change the Kd. Each stimulus increases the number of fibrinogen receptors in a dose-dependent manner, which correlates strongly (r = -0.98, n = 5) with an increased growth rate of cells in the presence of fibrinogen. This correlation concludes that the mitogenic effect of fibrinogen is controlled via receptor modulation.
 ...
PMID:Fibrinogen mitogenic effect on hemopoietic cell lines: control via receptor modulation. 301 35

The adenylate cyclase activator, forskolin, was found to induce expression of class I and class II major histocompatibility complex antigens in a B precursor cell line, Reh, as well as in a B lymphoid cell line, Raji. No such effect was, however, observed when the promyelocytic cells line HL-60 was treated with either forskolin or the cAMP analogue 8-bromoadenosine cyclic monophosphate. As expected, all three cell lines showed reduced proliferation upon forskolin treatment. Forskolin induced expression of class I and class II major histocompatibility complex antigens in cell lines not affected by interferon-gamma and vice versa, indicating that cAMP is not involved in the regulation of histocompatibility antigens by interferon-gamma. We also compared the effect of interferon-gamma and 12-O-tetradecanoylphorbol 13-acetate on major histocompatibility complex class I and class II expression, and despite differences in the response on the tested cell lines, we can not at this point exclude the possibility that protein kinase C is involved in the action of interferon-gamma.
 ...
PMID:Distinct effect of forskolin and interferon-gamma on cell proliferation and regulation of histocompatibility antigen expression in hematopoietic cells. 308 31

Addition of either ATP or ouabain to the culture medium markedly depressed thymidine incorporation into DNA in Raji cells. The electromagnetic field, pulsating at very low frequency, did not affect DNA synthesis in normal culture media nor did it alter its ouabain-inhibition, but it partially reversed the ATP-inhibition. In spite of the presence of ATP, ouabain prevented stimulation of ATPase and DNA synthesis by the field. Although no mechanism is known for the action of either ATP or the field, the results may be interpreted in light of existing speculations. In the absence of the field, external ATP may go into an ATP pool that either blocks ATPase or feeds adenyl cyclase, which hinders DNA synthesis. In contrast, the electromagnetic field may either turn off adenyl cyclase or simply stimulate the ATP-depressed ATPase.
 ...
PMID:Electromagnetic modulation of biological processes: ATPase function and DNA production by Raji cancer cells in vitro. 622 58

Vasoactive intestinal polypeptide (VIP) was found to be a potent stimulator of lymphocyte adenylate cyclase activity. VIP-induced activation of adenylate cyclase was specific for lymphocytes among peripheral blood cells; i.e., VIP did not stimulate the adenylate cyclase activity of neutrophils, monocytes, or platelets. The VIP-induced activation of lymphocyte adenylate cyclase was time, temperature, and concentration dependent. VIP and the GTP analog, Gpp(NH)p, acted synergistically to stimulate lymphocyte adenylate cyclase; stimulation by VIP and PGE1 was additive; and VIP activation was antagonized by somatostatin. VIP-mediated activation of lymphocyte adenylate cyclase was observed in normal human T cells, B cells obtained from a patient with chronic lymphocytic leukemia, and a human T cell culture line. The Raji human B cell culture line did possess adenylate cyclase activity, but this activity was not stimulated by VIP. These results suggest that lymphocytes possess functional receptors for VIP and that this peptide may play a role in modulation of lymphocyte function.
 ...
PMID:Vasoactive intestinal polypeptide modulation of lymphocyte adenylate cyclase. 697 28