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Gene Review

Ccna2  -  cyclin A2

Rattus norvegicus

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High impact information on Ccna2


Biological context of Ccna2

  • As a novel therapeutic strategy, the induction of endogenous myocardial regeneration was investigated by initiating cardiomyocyte mitosis by expressing the cell cycle regulator cyclin A2 [4].
  • Cyclin A2 animals manifested improved hemodynamics: Pmax (70.6+/-8.9 versus 60.4+/-11.8 mm Hg; P=0.017), max dP/dt (3000+/-588 versus 2500+/-643 mm Hg/sec; P<0.05), preload adjusted maximal power (5.75+/-4.40 versus 2.75+/-0.98 mWatts/microL2; P<0.05), and cardiac output (26.8+/-3.7 versus 22.7+/-2.6 mL/min; P=0.004) [4].
  • Messenger RNA (mRNA) and protein levels for cyclin A2 and G1, which are putative intracellular regulators of Leydig cell proliferation and differentiation, were measured by RT-PCR and immunoblotting, respectively [3].
  • The time-course of c-myc and cyclin A2 mRNA expression was determined in the liver of male Sprague-Dawley rats during transient liver cell proliferation induced by a single dose of ethinyl estradiol (EE), and was compared to that during liver regeneration following two-thirds hepatectomy (PH) [5].

Anatomical context of Ccna2

  • Cyclin A2 hearts demonstrated increased borderzone myofilament density (39.8+/-1.1 versus 31.8+/-1.0 cells/hpf; P=0.0011) [4].
  • METHODS AND RESULTS: Lewis rats underwent left anterior descending coronary artery ligation followed by peri-infarct intramyocardial delivery of adenoviral vector expressing cyclin A2 (n =32) or empty adeno-null (n =32) [4].

Associations of Ccna2 with chemical compounds


Other interactions of Ccna2

  • The promoter activity of cyclin A2 was 4-fold higher in Rat1a cells in which c-Jun expression was induced compared with the control cells [2].
  • Thus, our results suggest that c-Jun is a mediator of the aberrant cyclin A2 expression associated with Ras/Src-induced transformation [2].
  • Cyclin A2 mRNA levels, normalized to ribosomal protein S16 (RPS16), were highest in PLC (2.76 +/- 0.21, mean +/- SE), intermediate in ILC (1.79 +/- 0.14), and lowest in ALC (0.40 +/- 0.06) [3].

Analytical, diagnostic and therapeutic context of Ccna2


  1. S-adenosylmethionine regulates cytoplasmic HuR via AMP-activated kinase. Martínez-Chantar, M.L., Vázquez-Chantada, M., Garnacho, M., Latasa, M.U., Varela-Rey, M., Dotor, J., Santamaria, M., Martínez-Cruz, L.A., Parada, L.A., Lu, S.C., Mato, J.M. Gastroenterology (2006) [Pubmed]
  2. Cyclin A is a c-Jun target gene and is necessary for c-Jun-induced anchorage-independent growth in RAT1a cells. Katabami, M., Donninger, H., Hommura, F., Leaner, V.D., Kinoshita, I., Chick, J.F., Birrer, M.J. J. Biol. Chem. (2005) [Pubmed]
  3. Decreased cyclin A2 and increased cyclin G1 levels coincide with loss of proliferative capacity in rat Leydig cells during pubertal development. Ge, R.S., Hardy, M.P. Endocrinology (1997) [Pubmed]
  4. Therapeutic delivery of cyclin A2 induces myocardial regeneration and enhances cardiac function in ischemic heart failure. Woo, Y.J., Panlilio, C.M., Cheng, R.K., Liao, G.P., Atluri, P., Hsu, V.M., Cohen, J.E., Chaudhry, H.W. Circulation (2006) [Pubmed]
  5. Cyclin A2 and c-myc mRNA expression in ethinyl estradiol induced liver proliferation. Payraudeau, V., Sarsat, J.P., Sobczak, J., Bréchot, C., Albaladéjo, V. Mol. Cell. Endocrinol. (1998) [Pubmed]
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