Show simple item record

dc.contributor.authorMedepalli, Vidya
dc.date.accessioned2016-03-17T12:59:36Zen
dc.date.available2016-03-17T12:59:36Zen
dc.date.issued2016-03en
dc.identifier.urihttp://hdl.handle.net/10675.2/601938en
dc.descriptionPresentation given at the 17th Annual Phi Kappa Phi Student Research and Fine Arts Conferenceen
dc.description.abstractIntroduction and aim: Pancreatic adenocarcinoma is among the most aggressive of all cancers. Adenosine 3’, 5’ cyclic monophosphate (cyclic AMP) is involved in the internal cellular enzymatic activity and gene expression. It is found to be involved in the mechanism of pancreatic tumorigenesis. So far, two effectors for cyclic AMP are known; one is protein kinase A (PKA) and the other is an exchange protein directly activated by cAMP (EPAC). Our research group has found that AC1 is responsible for the inhibitory effect of Forskolin on cell proliferation of HPAC. My research project focuses on studying the effectors implicated in the inhibitory effect of activated AC1. Result: We were successfully able to overexpress AC1 using a plasmid human ADCY1 cDNA in pCMV-SPORT6. Through the overexpression, we were able to support the conclusion that AC1 inhibits cell proliferation in HPAC cells. We found that both H-89 (inhibitor of PKA) and ESI (inhibitor of EPAC) counteracts the effect of AC1. Conclusion: Both effectors- PKA and EPAC- mediate the inhibitory effect of AC1. Funding Source: Center for Undergraduate Research and Scholarship and Department of Biological Sciences, Scholarly Activity Award
dc.language.isoen_USen
dc.subjectPancreatic Neoplasmsen
dc.subjectAdenocarcinomaen
dc.subjectPlasmidsen
dc.titleEffectors Implicated In the Ac1 Inhibitory Effect on Cell Proliferation in Pancreatic Cancer Cellsen_US
dc.typePresentationen
dc.contributor.departmentDepartment of Biological Sciencesen
dc.description.advisorSabbatini, Mariaen
refterms.dateFOA2019-04-09T22:39:15Z
html.description.abstractIntroduction and aim: Pancreatic adenocarcinoma is among the most aggressive of all cancers. Adenosine 3’, 5’ cyclic monophosphate (cyclic AMP) is involved in the internal cellular enzymatic activity and gene expression. It is found to be involved in the mechanism of pancreatic tumorigenesis. So far, two effectors for cyclic AMP are known; one is protein kinase A (PKA) and the other is an exchange protein directly activated by cAMP (EPAC). Our research group has found that AC1 is responsible for the inhibitory effect of Forskolin on cell proliferation of HPAC. My research project focuses on studying the effectors implicated in the inhibitory effect of activated AC1. Result: We were successfully able to overexpress AC1 using a plasmid human ADCY1 cDNA in pCMV-SPORT6. Through the overexpression, we were able to support the conclusion that AC1 inhibits cell proliferation in HPAC cells. We found that both H-89 (inhibitor of PKA) and ESI (inhibitor of EPAC) counteracts the effect of AC1. Conclusion: Both effectors- PKA and EPAC- mediate the inhibitory effect of AC1. Funding Source: Center for Undergraduate Research and Scholarship and Department of Biological Sciences, Scholarly Activity Award


Files in this item

Thumbnail
Name:
vidya_pkp_oral_presentation_20 ...
Size:
1.349Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record