[1]Riaz S, Zeidan A, Mraiche F. Myocardial proteases and cardiac remodeling[J]. J Cell Physiol, 2017, 232(12): 3244-3250.
[2]Zhao L, Wu D, Sang M, et al. Stachydrine ameliorates isoproterenol-induced cardiac hypertrophy and fibrosis by suppressing inflammation and oxidative stress through inhibiting NF-kappaB and JAK/STAT signaling pathways in rats[J]. Int Immunopharmacol, 2017, 48: 102-109.
[3]Welch EJ, Jones BW, Scott JD. Networking with AKAPs: context-dependent regulation of anchored enzymes[J]. Mol Interv, 2010, 10(2): 86-97.
[4]Pawson CT, Scott JD. Signal integration through blending, bolstering and bifurcating of intracellular information[J]. Nat Struct Mol Biol, 2010, 17(6): 653-658.
[5]Scott JD, Dessauer CW, Tasken K. Creating order from chaos: cellular regulation by kinase anchoring[J]. Annu Rev Pharmacol Toxicol, 2013, 53: 187-210.
[6]Diviani D, Maric D, Perez Lopez I, et al. A-kinase anchoring proteins: molecular regulators of the cardiac stress response[J]. Biochim Biophys Acta, 2013, 1833(4): 901-908.
[7]Skroblin P, Grossmann S, Schafer G, et al. Mechanisms of protein kinase A anchoring[J]. Int Rev Cell Mol Biol, 2010, 283: 235-330.
[8]Beene DL, Scott JD. A-kinase anchoring proteins take shape[J]. Curr Opin Cell Biol, 2007, 19(2): 192-198.
[9]Carnegie GK, Burmeister BT. A-kinase anchoring proteins that regulate cardiac remodeling[J]. J Cardiovasc Pharmacol, 2011, 58(5): 451-458.
[10]Abrenica B, Alshaaban M, Czubryt MP. The A-kinase anchor protein AKAP121 is a negative regulator of cardiomyocyte hypertrophy[J]. J Mol Cell Cardiol, 2009, 46(5): 674-681.
[11]Carnegie GK, Soughayer J, Smith FD, et al. AKAP-Lbc mobilizes a cardiac hypertrophy signaling pathway[J]. Mol Cell, 2008, 32(2): 169-179.
[12] Perez Lopez I, Cariolato L, Maric D, et al. A-kinase anchoring protein Lbc coordinates a p38 activating signaling complex controlling compensatory cardiac hypertrophy[J]. Mol Cell Biol, 2013, 33(15): 2903-2917.
[13]Kritzer MD, Li J, Passariello CL, et al. The scaffold protein muscle A-kinase anchoring protein beta orchestrates cardiac myocyte hypertrophic signaling required for the development of heart failure[J]. Circ Heart Fail, 2014, 7(4): 663-672.
[14]Scott JD, Pawson T. Cell signaling in space and time: where proteins come together and when they're apart[J]. Science, 2009, 326(5957): 1220-1224.
[15]Rababa'h A, Craft JW Jr, Wijaya CS, et al. Protein kinase A and phosphodiesterase-4D3 binding to coding polymorphisms of cardiac muscle anchoring protein (mAKAP)[J]. J Mol Biol, 2013, 425(18): 3277-3288.
[16]Passariello CL, Li J, Dodge-Kafka K, et al. mAKAP-a master scaffold for cardiac remodeling[J]. J Cardiovasc Pharmacol, 2015, 65(3): 218-225.
[17]Zhang L, Malik S, Pang J, et al. Phospholipase Cepsilon hydrolyzes perinuclear phosphatidylinositol 4-phosphate to regulate cardiac hypertrophy[J]. Cell, 2013, 153(1): 216-227.
[18]Xie M, Hill JA. HDAC-dependent ventricular remodeling[J]. Trends Cardiovasc Med, 2013, 23(6): 229-235.
[19]Liu Q, Hofmann PA. Protein phosphatase 2A-mediated cross-talk between p38 MAPK and ERK in apoptosis of cardiac myocytes[J]. Am J Physiol Heart Circ Physiol, 2004, 286(6): H2204-H2212.
[20]Dodge-Kafka KL, Kapiloff MS. The mAKAP signaling complex: integration of cAMP, calcium, and MAP kinase signaling pathways[J]. Eur J Cell Biol, 2006, 85(7): 593-602.
[21]Li J, Kritzer MD, Michel JJ, et al. Anchored p90 ribosomal S6 kinase 3 is required for cardiac myocyte hypertrophy[J]. Circ Res, 2013, 112(1): 128-139.
[22]Martinez EC, Passariello CL, Li J, et al. RSK3: A regulator of pathological cardiac remodeling[J]. IUBMB Life, 2015, 67(5): 331-337.
[23]Cavin S, Maric D, Diviani D. A-kinase anchoring protein-Lbc promotes pro-fibrotic signaling in cardiac fibroblasts[J]. Biochim Biophys Acta, 2014, 1843(2): 335-345.
[24] Cariolato L, Cavin S, Diviani D. A-kinase anchoring protein (AKAP)-Lbc anchors a PKN-based signaling complex involved in alpha1-adrenergic receptor-induced p38 activation[J]. J Biol Chem, 2011, 286(10): 7925-7937.
[25]Marber MS, Rose B, Wang Y. The p38 mitogen-activated protein kinase pathway--a potential target for intervention in infarction, hypertrophy, and heart failure[J]. J Mol Cell Cardiol, 2011, 51(4): 485-490.
[26]Streicher JM, Ren S, Herschman H, et al. MAPK-activated protein kinase-2 in cardiac hypertrophy and cyclooxygenase-2 regulation in heart[J]. Circ Res, 2010, 106(8): 1434-1443.
[27]Del Vescovo CD, Cotecchia S, Diviani D. A-kinase-anchoring protein-Lbc anchors IkappaB kinase beta to support interleukin-6-mediated cardiomyocyte hypertrophy[J]. Mol Cell Biol, 2013, 33(1): 14-27.
[28]Smith FD, Scott JD. A-kinase-anchoring protein-Lbc connects stress signaling to cardiac hypertrophy[J]. Mol Cell Biol, 2013, 33(1): 2-3.
[29]Spindler MJ, Burmeister BT, Huang Y, et al. AKAP13 Rho-GEF and PKD-binding domain deficient mice develop normally but have an abnormal response to beta-adrenergic-induced cardiac hypertrophy[J]. PLoS One, 2013, 8(4): e62705.
[30]Taglieri DM, Johnson KR, Burmeister BT, et al. The C-terminus of the long AKAP13 isoform (AKAP-Lbc) is critical for development of compensatory cardiac hypertrophy[J]. J Mol Cell Cardiol, 2014, 66: 27-40.
[31]Johnson KR, Nicodemus-Johnson J, Spindler MJ, et al. Genome-wide gene expression analysis shows AKAP13-mediated PKD1 signaling regulates the transcriptional response to cardiac hypertrophy[J]. PLoS One, 2015, 10(7): e0132474.
[32]Barry SP, Townsend PA. What causes a broken heart-molecular insights into heart failure[J]. Int Rev Cell Mol Biol, 2010, 284: 113-179.
[33]Edwards HV, Scott JD, Baillie GS. The A-kinase-anchoring protein AKAP-Lbc facilitates cardioprotective PKA phosphorylation of Hsp20 on Ser(16)[J]. Biochem J, 2012, 446(3): 437-443.
[34]Schiattarella GG, Cattaneo F, Pironti G, et al. Akap1 deficiency promotes mitochondrial aberrations and exacerbates cardiac injury following permanent coronary ligation via enhanced mitophagy and apoptosis[J]. PLoS One, 2016, 11(5): e0154076. |