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Relevant bibliographies by topics / Receptor guanylyl cyclase C

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Academic literature on the topic 'Receptor guanylyl cyclase C'

Author: Grafiati

Published: 6 September 2023

Last updated: 7 September 2023

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Journal articles on the topic "Receptor guanylyl cyclase C"

1

Mann, E. A., M. B. Cohen, and R. A. Giannella. "Comparison of receptors for Escherichia coli heat-stable enterotoxin: novel receptor present in IEC-6 cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 1 (January 1, 1993): G172—G178. http://dx.doi.org/10.1152/ajpgi.1993.264.1.g172.

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Enterotoxigenic Escherichia coli elaborate a heat-stable enterotoxin that causes diarrhea in humans and animals. The primary event in the diarrheal cascade is the binding of this enterotoxin to specific receptors on enterocytes and activation of guanylyl cyclase. Two intestinal cell lines, Caco-2 and IEC-6, were tested for the presence of these receptors. Although both cell lines exhibited specific binding, only the Caco-2 cell line responded to heat-stable enterotoxin with increased guanylyl cyclase activity. Cloning and expression studies confirmed that the receptor present in Caco-2 cells is a homologue of guanylyl cyclase C, a known transmembrane heat-stable enterotoxin receptor. Expression of the receptor in differentiating Caco-2 cells increases with cell maturation, indicating that these cells are a suitable model for future studies. However, Northern and polymerase chain reaction analyses demonstrated that guanylyl cyclase C is not expressed in IEC-6 cells, strongly suggesting the presence of a novel heat-stable enterotoxin receptor that is not coupled to guanylyl cyclase activity.

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Trachte, G. J., S. Kanwal, B. J. Elmquist, and R. J. Ziegler. "C-type natriuretic peptide neuromodulates via "clearance" receptors." American Journal of Physiology-Cell Physiology 268, no. 4 (April 1, 1995): C978—C984. http://dx.doi.org/10.1152/ajpcell.1995.268.4.c978.

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A recently discovered endogenous autacoid, C-type natriuretic peptide, was tested in a pheochromocytoma (PC12) cell line for effects on 1) catecholamine release induced by a depolarizing stimulus, 2) guanylyl and adenylyl cyclase activities, and 3) specific 125I-labeled atrial natriuretic peptide (ANP) binding. C-type natriuretic peptide suppressed evoked neurotransmitter release in the absence of guanylyl cyclase activation or adenylyl cyclase inhibition; however, both a "clearance" (ANP-C) receptor binding agent, des-[Gln18Ser19Gly20Leu21Gly22]-ANF-(4-23)-NH2 (cANF), and pertussis toxin prevented this neuromodulatory effect. The C-type natriuretic peptide preferentially bound to receptors that also bound cANF. The results suggest that C-type natriuretic peptide suppressed evoked neurotransmitter efflux by binding to ANP-C receptors coupled to a pertussis toxin-sensitive process; furthermore, the neuromodulatory effect of C-type natriuretic peptide occurred independently of guanylyl cyclase activation or adenylyl cyclase inhibition. The novel aspects of these findings are 1) neuromodulatory effects of C-type natriuretic peptide, 2) guanylyl cyclase-independent actions of C-type natriuretic peptide, and 3) ANP-C receptors mediating C-type natriuretic peptide actions.

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Bhandari, Rashna, K. Suguna, and Sandhya S. Visweswariah. "Guanylyl Cyclase C Receptor: Regulation of Catalytic Activity by ATP." Bioscience Reports 19, no. 3 (June 1, 1999): 179–88. http://dx.doi.org/10.1023/a:1020273619211.

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Guanylyl cyclase C (GCC), a member of the family of membrane bound guanylyl cyclases is the receptor for the heat-stable enterotoxin (ST) peptides and the guanylin family of endogenous peptides. GCC is activated upon ligand binding to increase intracellular cGMP levels, which in turn activates other downstream signalling events in the cell. GCC is also activated in vitro by nonionic detergents. We have used the T84 cell line as a model system to investigate the regulation of GCC activity by ATP. Ligand-stimulated GCC activity is potentiated in the presence of ATP, whereas detergent-stimulated activity is inhibited. The potentiation of GCC activity by ATP is dependent on the presence of Mg2+ ions, and is probably brought about by a direct binding of Mg-ATP to GCC. The protein kinase-like domain of GCC, which has earlier been shown to play a critical role in the regulation of GCC activity, may be a possible site for the binding of Mg-ATP to GCC.

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Nighorn, A., P. J. Simpson, and D. B. Morton. "The novel guanylyl cyclase MsGC-I is strongly expressed in higher-order neuropils in the brain of Manduca sexta." Journal of Experimental Biology 204, no. 2 (January 15, 2001): 305–14. http://dx.doi.org/10.1242/jeb.204.2.305.

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Guanylyl cyclases are usually characterized as being either soluble (sGCs) or receptor (rGCs). We have recently cloned a novel guanylyl cyclase, MsGC-I, from the developing nervous system of the hawkmoth Manduca sexta that cannot be classified as either an sGC or an rGC. MsGC-I shows highest sequence identity with receptor guanylyl cyclases throughout its catalytic and dimerization domains, but does not contain the ligand-binding, transmembrane or kinase-like domains characteristic of receptor guanylyl cyclases. In addition, MsGC-I contains a C-terminal extension of 149 amino acid residues. In this paper, we report the expression of MsGC-I in the adult. Northern blots show that it is expressed preferentially in the nervous system, with high levels in the pharate adult brain and antennae. In the antennae, immunohistochemical analyses show that it is expressed in the cell bodies and dendrites, but not axons, of olfactory receptor neurons. In the brain, it is expressed in a variety of sensory neuropils including the antennal and optic lobes. It is also expressed in structures involved in higher-order processing including the mushroom bodies and central complex. This complicated expression pattern suggests that this novel guanylyl cyclase plays an important role in mediating cyclic GMP levels in the nervous system of Manduca sexta.

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Callahan, W., M. Forster, and T. Toop. "Evidence of a guanylyl cyclase natriuretic peptide receptor in the gills of the new zealand hagfish Eptatretus cirrhatus (Class Agnatha)." Journal of Experimental Biology 203, no. 17 (September 1, 2000): 2519–28. http://dx.doi.org/10.1242/jeb.203.17.2519.

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Natriuretic peptide binding sites were examined in the gills of the hagfish Eptatretus cirrhatus (Class Agnatha, subfamily Eptatretinae) using radio-ligand binding techniques, molecular cloning and guanylyl cyclase assays. Iodinated rat atrial natriuretic peptide ((125)I-rANP) and iodinated porcine C-type natriuretic peptide ((125)I-pCNP) bound specifically to the lamellar folds and cavernous tissue of E. cirrhatus gills, and 0.3 nmol l(−1) rat ANP competed for 50 % of specific (125)I-rANP binding sites. Affinity cross-linking of (125)I-rANP to gill membranes followed by sodium dodecylsulphate-polyacrylamide gel electrophoresis revealed a single binding site of 150 kDa. In the presence of Mn(2+), 0.1 nmol l(−1) rANP inhibited cGMP production, whereas 1 micromol l(−1) rANP stimulated cGMP production rates. At 1 micromol l(−1), pCNP also stimulated cGMP production. The production of cGMP was also measured in the presence and absence of ATP with either Mn(2+) or Mg(2+). Reverse transcriptase polymerase chain reaction (RT-PCR) of hagfish gill RNA, followed by cloning and sequencing of PCR products, produced a partial cDNA sequence of a natriuretic peptide guanylyl cyclase receptor. The deduced amino acid sequence indicated 87–91 % homology with other natriuretic peptide guanylyl cyclase receptors. This study indicates the presence of a natriuretic peptide guanylyl cyclase receptor in the gills of E. cirrhatus that is similar to the natriuretic peptide guanylyl cyclase receptors in higher vertebrates. These observations demonstrate that the coupling of natriuretic peptide receptors with guanylyl cyclase has a long evolutionary history.

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Guo, Lai-Jing, Abdel A. Alli, Douglas C. Eaton, and Hui-Fang Bao. "ENaC is regulated by natriuretic peptide receptor-dependent cGMP signaling." American Journal of Physiology-Renal Physiology 304, no. 7 (April 1, 2013): F930—F937. http://dx.doi.org/10.1152/ajprenal.00638.2012.

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Epithelial sodium channels (ENaCs) located at the apical membrane of polarized epithelial cells are regulated by the second messenger guanosine 3′,5′-cyclic monophosphate (cGMP). The mechanism for this regulation has not been completely characterized. Guanylyl cyclases synthesize cGMP in response to various intracellular and extracellular signals. We investigated the regulation of ENaC activity by natriuretic peptide-dependent activation of guanylyl cyclases in Xenopus 2F3 cells. Confocal microscopy studies show natriuretic peptide receptors (NPRs), including those coupled to guanylyl cyclases, are expressed at the apical membrane of 2F3 cells. Single-channel patch-clamp studies using 2F3 cells revealed that atrial natriuretic peptide (ANP) or 8-(4-chlorophenylthio)-cGMP, but not C-type natriuretic peptide or cANP, decreased the open probability of ENaC. This suggests that NPR-A, but not NPR-B or NPR-C, is involved in the natriuretic peptide-mediated regulation of ENaC activity. Also, it is likely that a signaling pathway involving cGMP and nitric oxide (NO) are involved in this mechanism, since inhibitors of soluble guanylyl cyclase, protein kinase G, inducible NO synthase, or an NO scavenger blocked or reduced the effect of ANP on ENaC activity.

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Mukaddam-Daher, S., J. Tremblay, N. Fujio, C. Koch, M. Jankowski, E. W. Quillen, and J. Gutkowska. "Alteration of lung atrial natriuretic peptide receptors in genetic cardiomyopathy." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 1 (July 1, 1996): L38—L45. http://dx.doi.org/10.1152/ajplung.1996.271.1.l38.

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These studies were designed to characterize the atrial natriuretic peptide (ANF) receptor subtypes [guanylyl cyclase natriuretic peptide receptors (NPR-A, NPR-B) and NPR-C] in lungs of normal hamsters and to evaluate alterations in receptor kinetics in genetic cardiomyopathy (CMO), a model of human congestive heart failure. Lung membranes were obtained from normal and CMO 200-to 230-day-old hamsters. Cross-linking and competitive binding receptor assays using 125I-labeled human ANF showed that lung membranes exhibit NPR, mainly guanylyl cyclase NPR-A and clearance NPR-C receptors. Stimulation of guanylyl cyclase by ANF and C-type natriuretic peptide (CNP) confirmed the presence of NPR-A and NPR-B. The maximum binding capacity of total ANF binding sites (442 +/- 68 vs. 271 +/- 57 fmol/mg protein, P < 0.05) was reduced, but dissociation constant (0.26 +/- 0.04 vs. 0.41 +/- 0.08 nM) was not altered in CMO animals. Similar reductions were observed in the binding sites for brain natriuretic peptide (BNP; 438 +/- 83 vs. 236 +/- 53 fmol/mg protein) and CNP (321 +/- 80 vs. 165 +/- 56 fmol/mg protein, P < 0.05) which may reflect a decline in NPR-A and NPR-B and/or NPR-C. Acid wash improved binding of 125I-labeled rat ANF to lung membranes of both normal and CMO hamsters, but the tendency towards reduced binding in CMO hamsters did not reach statistical significance, implying that downregulation may not have been due only to prior occupancy of the receptors. Transcripts of NPR-A, NPR-B, and NPR-C receptors in hamster lungs were detected by quantitative polymerase chain reaction. Compared with normal controls, the CMO hamster lung NPR-A mRNA was reduced by 50%, but NPR-B mRNA and NPR-C mRNA were not altered. Moreover, CMO hamster lungs showed less activation of guanylyl cyclase by ANF. These studies demonstrate that lung NPR are downregulated in hamster CMO.

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Bominaar, A. A., and P. J. Van Haastert. "Chemotactic antagonists of cAMP inhibit Dictyostelium phospholipase C." Journal of Cell Science 104, no. 1 (January 1, 1993): 181–85. http://dx.doi.org/10.1242/jcs.104.1.181.

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In Dictyostelium discoideum extracellular cAMP induces chemotaxis via a transmembrane signal transduction cascade consisting of surface cAMP receptors, G-proteins and effector enzymes including adenylyl cyclase, guanylyl cyclase and phospholipase C. Previously it was demonstrated that some cAMP derivatives such as 3′-deoxy-3′-aminoadenosine 3′:5′-monophosphate (3′NH-cAMP) bind to the receptor and induce normal activation of adenylyl cyclase and guanylyl cyclase. However these analogues do not induce chemotaxis, probably because the signal is transduced in an inappropriate manner. We have now studied the regulation of phospholipase C by cAMP and these chemotactic antagonists. cAMP induced the two-fold activation of phospholipase C leading to a transient increase of Ins(1,4,5)P3 levels. In contrast, the analogues induced a rapid decrease of intracellular Ins(1,4,5)P3 levels, due to the inhibition of phospholipase C activity. In a transformed cell-line lacking the G-protein that mediates phospholipase C inhibition, 3′NH-cAMP did not decrease phospholipase C activity and was no longer an antagonist of chemotaxis. These results suggest that inhibition of phospholipase C leads to aberrant chemotaxis.

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Carrithers, Stephen L., Cobern E. Ott, Michael J. Hill, Brett R. Johnson, Weiyan Cai, Jason J. Chang, Rajesh G. Shah, et al. "Guanylin and uroguanylin induce natriuresis in mice lacking guanylyl cyclase-C receptor." Kidney International 65, no. 1 (January 2004): 40–53. http://dx.doi.org/10.1111/j.1523-1755.2004.00375.x.

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Basu, Nirmalya, Najla Arshad, and Sandhya S. Visweswariah. "Receptor guanylyl cyclase C (GC-C): regulation and signal transduction." Molecular and Cellular Biochemistry 334, no. 1-2 (December 4, 2009): 67–80. http://dx.doi.org/10.1007/s11010-009-0324-x.

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Dissertations / Theses on the topic "Receptor guanylyl cyclase C"

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Nedvetsky, Pavel I. "Regulation of the nitric oxide receptor, soluble guanylyl cyclase." Doctoral thesis, [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969682026.

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Ogawa, Yoshihisa. "Natriuretic peptide receptor guanylyl cyclase-A protects podocytes from aldosterone-induced glomerular injury." Kyoto University, 2012. http://hdl.handle.net/2433/160971.

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Birnby, Deborah Ann. "Analysis of daf-11, a transmembrane guanylyl cyclase that mediates chemosensory transduction in C. elegans /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/10300.

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Ter-Avetisyan, Gohar [Verfasser]. "The receptor guanylyl cyclase Npr2 regulates the bifurcation of cranial sensory axons / Gohar Ter-Avetisyan." Berlin : Freie Universität Berlin, 2013. http://d-nb.info/104244143X/34.

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Nakanishi, Michio. "Role of natriuretic peptide receptor guanylyl cyclase-A in myocardial infarction evaluated using genetically engineered mice." Kyoto University, 2006. http://hdl.handle.net/2433/143854.

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Morita, Rinpei. "Atrial natriuretic peptide polarizes human dendritic cells toward a Th2-promoting phenotype through its receptor guanylyl cyclase-coupled receptor-A." Kyoto University, 2003. http://hdl.handle.net/2433/148481.

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Liu, Yong [Verfasser]. "Targeted guanylyl cyclase C for optimization of circulating colorectal cancer cells enrichment and isolation / Yong Liu." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1148425500/34.

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Yamashita, Yui. "Brain-specific natriuretic peptide receptor-B deletion attenuates high-fat diet-induced visceral and hepatic lipid deposition in mice." Kyoto University, 2016. http://hdl.handle.net/2433/217139.

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Kato, Yukiko. "Natriuretic peptide receptor guanylyl cyclase-A pathway counteracts glomerular injury evoked by aldosterone through p38 mitogen-activated protein kinase inhibition." Kyoto University, 2018. http://hdl.handle.net/2433/235033.

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Yasoda, Akihiro. "Natriuretic peptide regulation of endochondral ossification-Evidence for possible roles of the C-type natriuretic peptide/guanylyl cyclase-B pathway." Kyoto University, 1999. http://hdl.handle.net/2433/156998.

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本文データは平成22年度国立国会図書館の学位論文(博士)のデジタル化実施により作成された画像ファイルを基にpdf変換したものである
Kyoto University (京都大学)
0048
新制・課程博士
博士(医学)
甲第7759号
医博第2112号
新制||医||713(附属図書館)
UT51-99-G353
京都大学大学院医学研究科内科系専攻
(主査)教授中西重忠, 教授中村孝志, 教授中尾一和
学位規則第4条第1項該当

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Book chapters on the topic "Receptor guanylyl cyclase C"

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Vaandrager, Arie B. "Structure and function of the heat-stable enterotoxin receptor/guanylyl cyclase C." In Guanylate Cyclase, 73–83. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0927-1_5.

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Mishra, Vishwas, Somesh Nandi, and Sandhya S. Visweswariah. "Guanylyl Cyclase C." In Encyclopedia of Signaling Molecules, 2301–8. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_539.

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Mishra, Vishwas, Somesh Nandi, and Sandhya S. Visweswariah. "Guanylyl Cyclase C." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_539-1.

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Meigs, Thomas E., Alex Lyakhovich, Hoon Shim, Ching-Kang Chen, Denis J. Dupré, Terence E. Hébert, Joe B. Blumer, et al. "Guanylyl Cyclase C." In Encyclopedia of Signaling Molecules, 838–43. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_539.

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Foster, David C., David L. Garbers, and Barbara J. Wedel. "The Guanylyl Cyclase-A Receptor." In Natriuretic Peptides in Health and Disease, 21–33. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3960-4_2.

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Lowe, David G. "The Guanylyl Cyclase-B Receptor." In Natriuretic Peptides in Health and Disease, 35–50. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3960-4_3.

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Chang, Peter S., Terry Hyslop, and Scott A. Waldman. "Guanylyl Cyclase C as Biomarker." In General Methods in Biomarker Research and their Applications, 1–16. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-7740-8_34-1.

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Tremblay, Johanne, Richard Desjardins, David Hum, Jolanta Gutkowska, and Pavel Hamet. "Biochemistry and physiology of the natriuretic peptide receptor guanylyl cyclases." In Guanylate Cyclase, 31–47. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0927-1_2.

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Chang, Peter S., Terry Hyslop, and Scott A. Waldman. "Guanylyl Cyclase C as a Biomarker." In Biomarkers in Disease: Methods, Discoveries and Applications, 363–81. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7696-8_34.

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Koesling, Doris, and Ari Sitaramayya. "Soluble Guanylyl Cyclase: The Nitric Oxide Receptor." In Signal Transduction: Pathways, Mechanisms and Diseases, 337–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02112-1_18.

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Conference papers on the topic "Receptor guanylyl cyclase C"

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Ravix, J., R. D. Britt, A. M. Roesler, S. A. Wicher, L. Manlove, M. Thompson, C. M. Pabelick, and Y. S. Prakash. "Hyperoxia-Induced Soluble Guanylyl Cyclase (sGC) Dysfunction in Developing Airway Involves the Calcium Sensing Receptor (CaSR)." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2180.

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Pelta-Heller, Josh, David S. Zuzga, Scott A. Waldman, and Giovanni M. Pitari. "Abstract 1614: Guanylyl cyclase C signaling through vasodilator-stimulated phosphoprotein in lost in colon cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1614.

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Kraft, Crystal, Jieru Lin, Adam Snook, Gilbert Kim, and Scott Waldman. "Abstract 1712: Intestinal stem cell integrity is preserved through modulation of endoplasmic reticulum stress by guanylyl cyclase C." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1712.

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Hesterman, Jacob Y., Kelly D. Orcutt, Ozlem Yardibi, Jerome T. Mettetal, Shu-Wen Teng, Donna Cvet, Jack Hoppin, Thea Kalebic, and Daniel P. Bradley. "Abstract 4948: PET/CT clinical protocol design for the novel, first in class 68Ga labeled guanylyl cyclase C targeted peptide MLN6907 ([68Ga]MLN6907)." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4948.

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Almhanna, Khaldoun, David Wright, Teresa Macarulla Mercadé, Jean-Luc Van Laethem, Antonio Cubillo Gracian, Carmen Guillén-Ponce, Jason Faris, et al. "Abstract CT117: A phase II trial of TAK-264, a novel antibody-drug conjugate (ADC), in patients with pancreatic adenocarcinoma expressing guanylyl cyclase C (GCC)." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-ct117.

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Jakobs, K. H., P. Gierschik, and R. Grandt. "THE ROLE OF GTP-BINDING PROTEINS EXHIBITING GTPase ACTIVITY IN PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644773.

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Activation of platelets by agonists acting via cell surface-located receptors apparently involves as an early event in transmembrane signalling an interaction of the agonist-occupied receptor with a guanine nucleotide-binding regulatory protein (G-protein). The activated G-protein, then, transduces the information to the effector molecule, being responsible for the changes in intracellular second messengers. At least two changes in intracellular signal molecules are often found to be associated with platelet activation by agonists, i.e., increases in inositol trisphosphate and diacylglycerol levels caused by activation of a polyphosphoinositide-specific phospholipase C and decrease in cyclic AMP concentration caused by inhibition of adenylate cyclase.Both actions of platelet-activating agents apparently involve G-proteins as transducing elements. Generally, the function of a G-protein in signal transduction can be measured either by its ability to regulate the activity of the effector molecule (phospholipase C or adenylate cyclase) or the binding affinity of an agonist to its specific receptor or by the abitlity of the G-protein to bind and hydrolyze GTP or one of its analogs in response to agonist-activated receptors. Some platelet-activating agonists (e.g. thrombin) can cause both adenylate cyclase inhibition and phospholipase C activation, whereas others induce either inhibition of adenylate cyclase (e.g. α2-adrenoceptor agonists) or activation of phospholipase C (e.g. stable endoperoxide analogs) . It is not yet known whether the simultaneous activation of two signal transduction systems is due to activation of two separate G-proteins by one receptor, to two distinct receptors activating each a distinct G-protein or to activation of two effector molecules by one G-protein.For some of the G-proteins, rather specific compounds are available causing inactivation of their function. In comparison to Gs, the stimulatory G-protein of the adenylate cyclase system, the adenylate cyclase inhibitory Gi-protein is rather specifically inactivated by ADP-ribosylation of its a-subunit by pertussis toxin, “unfortunately” not acting in intact platelets, and by SH-group reactive agents such as N-ethylmaleimide and diamide, apparently also affecting the Giα-subunit. Both of these treatments completely block α2-adrenoceptor-induced GTPase stimulation and adenylate cyclase inhibition and also thrombin-induced inhibition of adenylate cyclase. In order to know whether the G-protein coupling receptors to phospholipase C is similar to or different from the Gi-protein, high affinity GTPase stimulation by agents known to activate phospholipase C was evaluated in platelet membranes. The data obtained indicated that GTPase stimulation by agents causing both adenylate cyclase inhibition and phospholipase C activation is reduced, but only partially, by the above mentioned Gi-inactivating agents, while stimulation of GTPase by agents stimulating only phospholipase C is not affected by these treatments. These data suggested that the G-protein regulating phospholipase C activity in platelet membranes is different from the Gi-protein and may also not be a substrate for pertussis toxin. Measuring thrombin stimulation of inositol phosphate and diacylglycerol formation in saponin-permeabilized platelets, apparently contradictory data were reported after pertussis toxin treatment, being without effect or causing even an increase in thrombin stimulation of inositol phosphate formation (Lapetina: BBA 884, 219, 1986) or being inhibitory to thrombin stimulation of diacylglycerol formation (Brass et al.: JBC 261, 16838, 1986). These data indicate that the nature of the phospholipase C-related G-protein(s) is not yet defined and that their elucidation requires more specific tools as well as purification and reconstitution experiments. Preliminary data suggest that some antibiotics may serve as useful tools to characterize the phospho-lipase-related G-proteins. The possible role of G-protein phosphorylation by intracellular signal molecule-activated protein kinases in attenuation of signal transduction in platelets will be discussed.

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Teng, Shu-Wen, Christopher Zopf, Johnny Yang, Brad Stringer, Julie Zhang, Wen Chyi Shyu, Arijit Chakravarty, Petter Veiby, and Jerome Mettetal. "Abstract 4649: Using pharmacokinetic/efficacy modeling to identify the optimal schedule for MLN0264, an anti- guanylyl cyclase C (GCC) antibody-drug conjugate, in a range of xenograft models." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4649.

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Almhanna, Khaldoun, Maria Luisa Limon Miron, David Wright, Antonio Cubillo Gracian, Richard Hubner, Jean-Luc Van Laethem, Carolina Muriel López, et al. "Abstract CT107: Phase II trial of TAK-264 in previously treated patients (pts) with metastatic or recurrent adenocarcinoma of the stomach or gastroesophageal junction expression guanylyl cyclase C (GCC)." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-ct107.

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Cvet, Donna, Robert Robertson, Melissa Saylor, Jennifer Terkelsen, Ozlem Yardibi, Maria Borland, Nicolas Salem, et al. "Abstract 4949: In vitro and in vivo investigation of the novel, first-in-class, Guanylyl Cyclase C (GCC) targeted 68Ga labeled heat stable peptide MLN6907 ([68Ga]MLN6907) for tumor imaging." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4949.

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Koenig, Erik M., Cong Li, Huyuan Yang, Andy Zhu, Pooja Shah, Kazuho Nishimura, Bret Bannerman, et al. "Abstract 3916: Relationship of guanylyl cyclase C (GCC) expression and efficacy of TAK-164, a GCC-targeted antibody-drug conjugate in a panel of 68 subcutaneous HuPrime colorectal cancer PDX models." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3916.

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