1 Nagy A. Cre recombinase: The universal reagent for genome tailoring. Genesis, 2000, 26: 99-109？？
[2]
2 Gu H, Marth J D, Orban Pr C, et al. Deletion of a DNA polymerase beta gene segment in T cells using cell type-specific gene targeting.Science, 1994, 265: 103-106？？
[3]
3 Lakso M, Sauer B, Mosinger B, et al. Targeted oncogene activation by site-specific recombination in transgenic mice. Proc Natl Acad SciUSA, 1992, 89: 6232-6236？？
11 Derynck R, Zhang Y E. Smad-dependent and Smad-independent pathways in TGF-beta family signalling. Nature, 2003, 425: 577-584？？
[12]
12 Gaussin V, Van de Putte T, Mishina Y, et al. Endocardial cushion and myocardial defects after cardiac myocyte-specific conditionaldeletion of the bone morphogenetic protein receptor ALK3. Proc Natl Acad Sci USA, 2002, 99: 2878-2883？？
[13]
13 Monzen K, Shiojima I, Hiroi Y, et al. Bone morphogenetic proteins induce cardiomyocyte differentiation through the mitogen-activatedprotein kinase kinase kinase TAK1 and cardiac transcription factors Csx/Nkx-2.5 and GATA-4. Mol Cell Biol, 1999, 19: 7096-7105
[14]
14 Hamada H, Meno C, Watanabe D, et al. Establishment of vertebrate left-right asymmetry. Nat Rev Genet, 2002, 3: 103-113
[15]
15 Mikhailov A T, Torrado M. Shaping the Heart in Development and Disease. Kerala: Transworld Research Network, 2010. 117-144
[16]
16 Xu J, Kimball T R, Lorenz J N, et al. GDF15/MIC-1 functions as a protective and antihypertrophic factor released from the myocardium inassociation with SMAD protein activation. Circ Res, 2006, 98: 342-350？？
[17]
17 Chen H, Yong W, Ren S, et al. Overexpression of bone morphogenetic protein 10 in myocardium disrupts cardiac postnatal hypertrophicgrowth. J Biol Chem, 2006, 281: 27481-27491？？
[18]
18 Pardali E, Goumans M J, ten Dijke P. Signaling by members of the TGF-beta family in vascular morphogenesis and disease. Trends CellBiol, 2010, 20: 556-567？？
[19]
19 Yang X, Castilla L H, Xu X, et al. Angiogenesis defects and mesenchymal apoptosis in mice lacking SMAD5. Development, 1999, 126:1571-1580
[20]
20 Daneman R, Zhou L, Kebede A A, et al. Pericytes are required for blood-brain barrier integrity during embryogenesis. Nature, 2010, 468:562-566？？
[21]
21 Frese K K, Tuveson D A. Maximizing mouse cancer models. Nat Rev Cancer, 2007, 7: 645-658
[22]
22 Ding Z, Wu C J, Chu G C, et al. SMAD4-dependent barrier constrains prostate cancer growth and metastatic progression. Nature, 2011, 470:269-273？？
[23]
23 Xu X, Ehdaie B, Ohara N, et al. Synergistic action of Smad4 and Pten in suppressing pancreatic ductal adenocarcinoma formation in mice.Oncogene, 2010, 29: 674-686？？
[24]
24 Xu X, Kobayashi S, Qiao W, et al. Induction of intrahepatic cholangiocellular carcinoma by liver-specific disruption of Smad4 and Pten inmice. J Clin Invest, 2006, 116: 1843-1852？？
[25]
25 van de Laar I M, Oldenburg R A, Pals G, et al. Mutations in SMAD3 cause a syndromic form of aortic aneurysms and dissections withearly-onset osteoarthritis. Nat Genet, 2011, 43: 121-126？？
