Abstract

In previous years we had disrupted the genes encoding the pertussis toxin sensitive G proteins Gi2, Gi1, Gi3 and Go. Conditional knockouts for Gi2 and Go were also generated. Double knockouts involving Gi2 and Go are lethal. We expect to learn from combining Gi2 with Gi3 and enhanced survival of Go KO mice by removing the floxed genes at various times after birth. Breeding programs have been set up to add cre recombinase under several specific promoters so as to remove the genes both generally in all issues or in specific cell types such as in dopaminergic neurons to remove Go or lymphocytes to remove Gi from Gi3 KO mice. Most phenotypic studies were done in collaboration with outside investigators, Progress in this project was low and unsatisfactory andwas discontinued between Dec 15, 2013 and March 31, 2014.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Investigator-Initiated Intramural Research Projects (ZIA)
Project #
1ZIAES101643-12
Application #
8929779
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
12
Fiscal Year
2014
Total Cost
Indirect Cost

  Institution

Name
U.S. National Inst of Environ Hlth Scis
Department
Type
DUNS #
City
State
Country
Zip Code

  Publications

Choi, Chan-Il; Yoon, Sang-Phil; Choi, Jung-Mi et al. (2014) Simultaneous deletion of floxed genes mediated by CaMKII?-Cre in the brain and in male germ cells: application to conditional and conventional disruption of Go?. Exp Mol Med 46:e93
Ilatovskaya, Daria V; Palygin, Oleg; Chubinskiy-Nadezhdin, Vladislav et al. (2014) Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli. Kidney Int 86:506-14
Xia, Yang; Yang, Xiao-Ru; Fu, Zhenzhen et al. (2014) Classical transient receptor potential 1 and 6 contribute to hypoxic pulmonary hypertension through differential regulation of pulmonary vascular functions. Hypertension 63:173-80
Solanki, Sumeet; Dube, Prabhatchandra R; Tano, Jean-Yves et al. (2014) Reduced endoplasmic reticulum stress-induced apoptosis and impaired unfolded protein response in TRPC3-deficient M1 macrophages. Am J Physiol Cell Physiol 307:C521-31
Wang, Zhanwei; Dela Cruz, Rica; Ji, Fang et al. (2014) G(i)? proteins exhibit functional differences in the activation of ERK1/2, Akt and mTORC1 by growth factors in normal and breast cancer cells. Cell Commun Signal 12:10
Seo, Kinya; Rainer, Peter P; Lee, Dong-Ik et al. (2014) Hyperactive adverse mechanical stress responses in dystrophic heart are coupled to transient receptor potential canonical 6 and blocked by cGMP-protein kinase G modulation. Circ Res 114:823-32
Du, Juan; Ma, Xin; Shen, Bing et al. (2014) TRPV4, TRPC1, and TRPP2 assemble to form a flow-sensitive heteromeric channel. FASEB J 28:4677-85
Phelan, Kevin D; Shwe, U Thaung; Abramowitz, Joel et al. (2014) Critical role of canonical transient receptor potential channel 7 in initiation of seizures. Proc Natl Acad Sci U S A 111:11533-8
Shi, Jian; Birnbaumer, Lutz; Large, William A et al. (2014) Myristoylated alanine-rich C kinase substrate coordinates native TRPC1 channel activation by phosphatidylinositol 4,5-bisphosphate and protein kinase C in vascular smooth muscle. FASEB J 28:244-55
Liao, Yanhong; Abramowitz, Joel; Birnbaumer, Lutz (2014) The TRPC family of TRP channels: roles inferred (mostly) from knockout mice and relationship to ORAI proteins. Handb Exp Pharmacol 223:1055-75

Showing the most recent 10 out of 46 publications