| upregulation of CPI-17-mediated calcium-sensitized vasocontraction by obesity contributes to the development of obesity-related hypertension | CPI-17-mediated contraction of vascular smooth muscle is essential for the development of hypertension in obese mice.
Sun J, Tao T, Zhao W, Wei L, She F, Wang P, Li Y, Zheng Y, Chen X, Wang W, Qiao Y, Zhang XN, Zhu MS. | 05/16/2020 |
| These data provide a novel mechanism of the transcriptional control of CPI-17 in vascular smooth muscle cells under inflammatory conditions. Mechanistically, 2 GC boxes were identified as TNF response element in the CPI-17 promoter and KLF4 was upregulated by TNF, competed with Sp1 for the binding to the GC boxes in the CPI-17 promoter, and repressed CPI-17 transcription through histone deacetylase. | Transcriptional Suppression of CPI-17 Gene Expression in Vascular Smooth Muscle Cells by Tumor Necrosis Factor, Krüppel-Like Factor 4, and Sp1 Is Associated with Lipopolysaccharide-Induced Vascular Hypocontractility, Hypotension, and Mortality.
Zhao G, Zhong Y, Su W, Liu S, Song X, Hou T, Mu X, Gong MC, Guo Z., Free PMC Article | 01/25/2020 |
| CPI-17 phosphorylation at T38 is essential for the maintenance of physiological blood pressure. | The essential role of phospho-T38 CPI-17 in the maintenance of physiological blood pressure using genetically modified mice.
Yang Q, Fujii W, Kaji N, Kakuta S, Kada K, Kuwahara M, Tsubone H, Ozaki H, Hori M. | 12/22/2018 |
| Enhanced vasorelaxation in early endotoxemia is mediated by redox signaling through PKG-1alpha but in later endotoxemia by myosin phosphatase isoform shifts enhancing sensitivity to NO/cGMP as well as smooth muscle atrophy. | Redox signaling and splicing dependent change in myosin phosphatase underlie early versus late changes in NO vasodilator reserve in a mouse LPS model of sepsis.
Reho JJ, Zheng X, Asico LD, Fisher SA., Free PMC Article | 07/25/2015 |
| The study characterized the CPI-17 promoter and identified binding sites for GATA-6 and nuclear factor kappa B (NF-kappaB). | GATA-6 and NF-κB activate CPI-17 gene transcription and regulate Ca2+ sensitization of smooth muscle contraction.
Boopathi E, Hypolite JA, Zderic SA, Gomes CM, Malkowicz B, Liou HC, Wein AJ, Chacko S., Free PMC Article | 04/13/2013 |
| a novel signaling cascade that links RhoA-mediated calcium sensitivity to MEF2-dependent myocardin expression in VSMCs through a mechanism involving p38 MAPK, PP1alpha, and CPI-17. | A novel RhoA/ROCK-CPI-17-MEF2C signaling pathway regulates vascular smooth muscle cell gene expression.
Pagiatakis C, Gordon JW, Ehyai S, McDermott JC., Free PMC Article | 05/5/2012 |
| Data suggest that CPI-17 and both conventional and novel PKC isozymes contribute to the phasic and tonic contractile components of BALB/c colonic circular smooth muscle. | The contribution of protein kinase C and CPI-17 signaling pathways to hypercontractility in murine experimental colitis.
Ihara E, Chappellaz M, Turner SR, MacDonald JA. | 04/14/2012 |
| Organ-specific mechanisms involving MYPT1, M-RIP, and CPI-17 are critical to regulating basal LC20 phosphorylation in gastrointestinal smooth muscles. | Regulation of basal LC20 phosphorylation by MYPT1 and CPI-17 in murine gastric antrum, gastric fundus, and proximal colon smooth muscles.
Bhetwal BP, An CL, Fisher SA, Perrino BA., Free PMC Article | 01/14/2012 |
| calcium-independent phospholipase A2beta has a role in high glucose-induced activation of RhoA, Rho kinase, and CPI-17 in cultured vascular smooth muscle cells and vascular smooth muscle hypercontractility in diabetic animals | Role of calcium-independent phospholipase A2beta in high glucose-induced activation of RhoA, Rho kinase, and CPI-17 in cultured vascular smooth muscle cells and vascular smooth muscle hypercontractility in diabetic animals.
Xie Z, Gong MC, Su W, Xie D, Turk J, Guo Z., Free PMC Article | 04/19/2010 |
| CPI-17 expression is reversibly controlled in response to the phenotype transition of smooth muscle cells that restricts the signal to differentiated smooth muscle cells and particular cell types. | Expression of CPI-17 in smooth muscle during embryonic development and in neointimal lesion formation.
Kim JI, Young GD, Jin L, Somlyo AV, Eto M., Free PMC Article | 01/21/2010 |
| findings suggest that CPI-17 was downregulated during intestinal inflammation and that TNF-alpha plays a central role in this process. Downregulation of CPI-17 may play a role in motility impairments in inflammation. | Intestinal inflammation downregulates smooth muscle CPI-17 through induction of TNF-alpha and causes motility disorders.
Ohama T, Hori M, Momotani E, Iwakura Y, Guo F, Kishi H, Kobayashi S, Ozaki H. | 01/21/2010 |
| distribution of mouse and rat PPP1R14A was more specific and different from that of humans | Identification of human, mouse and rat PPP1R14A, protein phosphatase-1 inhibitor subunit 14A, & mapping human PPP1R14A to chromosome 19q13.13-q13.2.
Li Z, Yu L, Zhang Y, Gao J, Zhang P, Wan B, Chen C, Zhao S. | 01/21/2010 |
| concluded that actions downstream of cGMP/PKG can reverse PKC-mediated phosphorylation of CPI-17 and Ca(2+) sensitization in smooth muscle | Actions downstream of cyclic GMP/protein kinase G can reverse protein kinase C-mediated phosphorylation of CPI-17 and Ca²⁺ sensitization in smooth muscle.
Bonnevier J, Arner A. | 01/21/2010 |