[1]姜志华, 朱婉茹, 徐世永, 陈 杰, 黄瑞华, 刘红林, Archibald A L, Haley C S. 太湖猪种质基因特征研究. 南京农业大学学报, 2005, 28(2): 69-74. Jiang Z H, Zhu W R, Xu S Y, Chen J, Huang R H, Liu H L, Archibald A L, Haley C S. Molecular germ-plasm characteristics of Taihu pigs. Journal of Nanjing Agricultural University, 2005, 28(2): 69-74. (in Chinese)[2]Moustakas A, Souchelnytskyi S, Heldin C H. Smad regulation in TGF-β signal transduction. Journal of Cell Science, 2001, 114(24): 4359-4369.[3]Inui M, Manfrin A, Mamidi A, Martello G, Morsut L, Soligo S, Enzo E, Moro S, Polo S, Dupont S, Cordenonsi M, Piccolo S. USP15 is a deubiquitylating enzyme for receptor-activated SMADs. Nature Cell Biology, 2011, 13: 1368-1375. [4]Wang W, Chen X, Li X, Wang L, Zhang H, He Y, Wang J, Zhao Y, Zhang B, Xu Y. Interference RNA-based silencing of endogenous SMAD4 in porcine granulosa cells resulted in decreased FSH-mediated granulosa cells proliferation and steroidogenesis. Reproduction, 2011, 141(5): 643-651. [5]Pangas S A, Li X, Robertson E J, Matzuk M M. Premature luteinization and cumulus cell defects in ovarian-specific Smad4 knockout mice. Molecular Endocrinology, 2006, 20(6): 1406-1422. [6]Yao G, Yin M, Lian J, Tian H, Liu L, Li X, Sun F. MicroRNA-224 is involved in transforming growth factor-beta-mediated mouse granulosa cell proliferation and granulosa cell function by targeting Smad4. Molecular Endocrinology, 2010, 24(3): 540-551. [7]Pangas S A. Bone morphogenetic protein signaling transcription factor (SMAD) function in granulosa cells. Molecular and Cell Endocrinology, 2011. doi:10.1016/j.mce.2011.06.021[8]Li X, Tripurani S, James R, Pangas S A. Minimal fertility defects in mice deficient in oocyte-expressed Smad4. Biology of Reproduction, 2011. Doi: 10.1095/biolreprod.111.094375.[9]Sirard C, de la Pompa J L, Elia A, Itie A, Mirtsos C, Cheung A, Hahn S, Wakeham A, Schwartz L, Kern S E, Rossant J, Mak T W. The tumor suppressor gene Smad4/Dpc4 is required for gastrulation and later for anterior development of the mouse embryo. Genes and Development, 1998, 12(1): 107-119.[10]Yang X, Li C, Xu X, Deng C. The tumor suppressor SMAD4/DPC4 is essential for epiblast proliferation and mesoderm induction in mice. Proceedings of the National Academy of Sciences of the United States of America, 1998, 95(7): 3667-3672.[11]Gueripel X, Brun V, Gougeon A. Oocyte bone morphogenetic protein 15, but not growth differentiation factor 9, is increased during gonadotropin-induced follicular development in the immature mouse and is associated with cumulus oophorus expansion. Biology of Reproduction, 2006, 75(6): 836-843.[12]Xu Y, Li E, Han Y, Chen L, Xie Z. Differential expression of mRNAs encoding BMP/Smad pathway molecules in antral follicles of high- and low-fecundity Hu sheep. Animal Reproduction Science, 2010, 120: 47-55.[13]Tamura K, Dudley J, Nei M, Kumar S. MEGA4: molecular evolutionary genetics analysis (MEGA) software version 4.0. Molecular Biology and Evolution, 2007, 24(8): 1596-1599.[14]Librado P, Rozas J. DnaSP v5: A software for comprehensive analysis of DNA polymorphism data. Bioinformatics, 2009, 25(11): 1451-1452.[15]Knight A, Mindell D. Substitutions, weighting of DNA sequence evolution, and the phylogeny position of feaps viper. Systematic Biology, 1993, 42: 18-31.[16]Zhang Y, Feng X, We R, Derynck R. Receptor-associated mad homologues synergize as effectors of the TGF-beta response. Nature, 1996, 383(6596): 168-172.[17]Baburajendran N, Jauch R, Tan CY, Narasimhan K, Kolatkar P R. Structural basis for the cooperative DNA recognition by Smad4 MH1 dimers. Nucleic Acids Research, 2011, 39(18): 8213-8222.[18]Goto K, Kamiya Y, Imamura T, Miyazono K, Miyazawa K. Selective inhibitory effects of Smad6 on bone morphogenetic protein type I receptors. The Journal of Biological Chemistry, 2007, 282(28): 20603-20611.[19]Kaivo-oja N, Jeffery L A, Ritvos O, Mottershead D G. Smad signalling in the ovary. Reproductive Biology and Endocrinology, 2006, 4: 21-33.[20]Kaneko S, Chen X, Lu P, Yao X, Wright T G, Rajurkar M, Kariya K, Mao J, Ip Y T, Xu L. Smad inhibition by the Ste20 kinase Misshapen. Proceedings of the National Academy of Sciences of the United States of America, 2011, 108(27): 11127-11132. [21]Massagu J, Gomis R R. The logic of TGFbeta signaling. FEBS Letters, 2006, 580(12): 2811-2820.[22]Hata A, Lagna G, Massague J, Hemmati-Brivanlou A. Smad6 inhibits BMP/Smad1 signaling by specifically competing with the Smad4 tumor suppressor. Genes and Development, 1998, 12(2): 186-197.[23]da Silva S, Hasegawa H, Scott A, Zhou X, Wagner A K, Han B X, Wang F. Proper formation of whisker barrelettes requires periphery-derived Smad4-dependent TGF-β signaling. Proceedings of the National Academy of Sciences of the United States of America, 2011, 108(8): 3395-33400[24]Sirard C, de la Pompa J L, Elia A, Itie A, Mirtsos C, Cheung A, Hahn S, Wakeham A, Schwartz L, Kern S E, Rossant J, Mak T W. The tumor suppressor gene Smad4/Dpc4 is required for gastrulation and later for anterior development of the mouse embryo. Genes and Development, 1998, 12(1): 107-119.[25]Yang G, Yang X. Smad4-mediated TGF-β signaling in tumorigenesis. International Journal of Biological Sciences, 2010, 6(1): 1-8.[26]Le Goff C, Mahaut C, Abhyankar A, le Goff W, Serre V, Afenjar A, Destrée A, di Rocco M, Héron D, Jacquemont S, Marlin S, Simon M, Tolmie J, Verloes A, Casanova J L, Munnich A, Cormier-Daire V. Mutations at a single codon in mad homology 2 domain of SMAD4 cause Myhre syndrome. Nature Genetics, 2011, 44(1): 85-88.[27]Li J, Huang X, Xu X, Mayo J, Bringas P, Jiang R, Wang S, Chai Y. SMAD4-mediated WNT signaling controls the fate of cranial neural crest cells during tooth morphogenesis. Development, 2011, 138(10): 1977-1989. [28]Zhang C P, Yang J L, Zhang J, Li L, Huang L, Ji S Y, Hu Z Y, Gao F, Liu Y X. Notch signaling is involved in ovarian follicle development by regulating granulosa cell proliferation. Endocrinology, 2011, 152(6): 2437-2447. [29]Yu J, Yaba A, Kasiman C, Thomson T, Johnson J. mTOR controls ovarian follicle growth by regulating granulosa cell proliferation. PLoS One, 2011, 6(7): e21415. |