Balligand JL - Search Results

1

Regulation of cardiac myocyte contractile function by inducible nitric oxide synthase (iNOS): mechanisms of contractile depression by nitric oxide.

Joe EK, Schussheim AE, Longrois D, Mäki T, Kelly RA, Smith TW, Balligand JL. Joe EK, et al. Among authors: balligand jl. J Mol Cell Cardiol. 1998 Feb;30(2):303-15. doi: 10.1006/jmcc.1997.0593. J Mol Cell Cardiol. 1998. PMID: 9515007

2

Glucocorticoids increase osteopontin expression in cardiac myocytes and microvascular endothelial cells. Role in regulation of inducible nitric oxide synthase.

Singh K, Balligand JL, Fischer TA, Smith TW, Kelly RA. Singh K, et al. Among authors: balligand jl. J Biol Chem. 1995 Nov 24;270(47):28471-8. doi: 10.1074/jbc.270.47.28471. J Biol Chem. 1995. PMID: 7499354 Free article.

3

Cytokine-inducible nitric oxide synthase (iNOS) expression in cardiac myocytes. Characterization and regulation of iNOS expression and detection of iNOS activity in single cardiac myocytes in vitro.

Balligand JL, Ungureanu-Longrois D, Simmons WW, Pimental D, Malinski TA, Kapturczak M, Taha Z, Lowenstein CJ, Davidoff AJ, Kelly RA, et al. Balligand JL, et al. J Biol Chem. 1994 Nov 4;269(44):27580-8. J Biol Chem. 1994. PMID: 7525557 Free article.

4

Myocardial contractile dysfunction in the systemic inflammatory response syndrome: role of a cytokine-inducible nitric oxide synthase in cardiac myocytes.

Ungureanu-Longrois D, Balligand JL, Kelly RA, Smith TW. Ungureanu-Longrois D, et al. Among authors: balligand jl. J Mol Cell Cardiol. 1995 Jan;27(1):155-67. doi: 10.1016/s0022-2828(08)80015-6. J Mol Cell Cardiol. 1995. PMID: 7539082 Review.

5

Nitric oxide-dependent parasympathetic signaling is due to activation of constitutive endothelial (type III) nitric oxide synthase in cardiac myocytes.

Balligand JL, Kobzik L, Han X, Kaye DM, Belhassen L, O'Hara DS, Kelly RA, Smith TW, Michel T. Balligand JL, et al. J Biol Chem. 1995 Jun 16;270(24):14582-6. doi: 10.1074/jbc.270.24.14582. J Biol Chem. 1995. PMID: 7540173 Free article.

6

Contractile responsiveness of ventricular myocytes to isoproterenol is regulated by induction of nitric oxide synthase activity in cardiac microvascular endothelial cells in heterotypic primary culture.

Ungureanu-Longrois D, Balligand JL, Okada I, Simmons WW, Kobzik L, Lowenstein CJ, Kunkel SL, Michel T, Kelly RA, Smith TW. Ungureanu-Longrois D, et al. Among authors: balligand jl. Circ Res. 1995 Sep;77(3):486-93. doi: 10.1161/01.res.77.3.486. Circ Res. 1995. PMID: 7543825

7

Induction of nitric oxide synthase activity by cytokines in ventricular myocytes is necessary but not sufficient to decrease contractile responsiveness to beta-adrenergic agonists.

Ungureanu-Longrois D, Balligand JL, Simmons WW, Okada I, Kobzik L, Lowenstein CJ, Kunkel SL, Michel T, Kelly RA, Smith TW. Ungureanu-Longrois D, et al. Among authors: balligand jl. Circ Res. 1995 Sep;77(3):494-502. doi: 10.1161/01.res.77.3.494. Circ Res. 1995. PMID: 7543826

8

Control of cardiac muscle cell function by an endogenous nitric oxide signaling system.

Balligand JL, Kelly RA, Marsden PA, Smith TW, Michel T. Balligand JL, et al. Proc Natl Acad Sci U S A. 1993 Jan 1;90(1):347-51. doi: 10.1073/pnas.90.1.347. Proc Natl Acad Sci U S A. 1993. PMID: 7678347 Free PMC article.

9

Abnormal contractile function due to induction of nitric oxide synthesis in rat cardiac myocytes follows exposure to activated macrophage-conditioned medium.

Balligand JL, Ungureanu D, Kelly RA, Kobzik L, Pimental D, Michel T, Smith TW. Balligand JL, et al. J Clin Invest. 1993 May;91(5):2314-9. doi: 10.1172/JCI116461. J Clin Invest. 1993. PMID: 8486792 Free PMC article.

10

Regulation of cytokine-inducible nitric oxide synthase in cardiac myocytes and microvascular endothelial cells. Role of extracellular signal-regulated kinases 1 and 2 (ERK1/ERK2) and STAT1 alpha.

Singh K, Balligand JL, Fischer TA, Smith TW, Kelly RA. Singh K, et al. Among authors: balligand jl. J Biol Chem. 1996 Jan 12;271(2):1111-7. doi: 10.1074/jbc.271.2.1111. J Biol Chem. 1996. PMID: 8557638 Free article.

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