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2008 | 49 | 3 |

Tytuł artykułu

Isolation, sequence identification and tissue expression profiles of 3 novel porcine genes: ASPA, NAGA, and HEXA

Autorzy

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
The complete coding sequences of 3 porcine genes -ASPA, NAGA, and HEXA - were amplified by the reverse transcriptase polymerase chain reaction (RT-PCR) based on the conserved sequence information of the mouse or other mammals and referenced pig ESTs. These 3 novel porcine genes were then deposited in the NCB1 database and assigned GeneIDs: 100142661,100142664 and 100142667. The phylogenetic tree analysis revealed that the porcine ASPA, NAGA, and HEXA all have closer genetic relationships with theASPA, NAGA, and HEXA of cattle. Tissue expression profile analysis was also carried out and results revealed that swine ASPA, NAGA, and HEXA genes were differentially expressed in various organs, including skeletal muscle, the heart, liver, fat, kidney, lung, and small and large intestines. Our experiment is the first one to establish the foundation for further research on these 3 swine genes.

Słowa kluczowe

Wydawca

-

Rocznik

Tom

49

Numer

3

Opis fizyczny

p.257-261,fig.,ref.

Twórcy

autor
  • College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China
autor
  • College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China
autor
  • College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China
autor
  • College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China
autor
  • Key Laboratory of Animal Nutrition and Feed of Yunnan Province, Yunnan Agricultural University, Kunming, China

Bibliografia

  • Chabás A, Duque J, Gort L, 2007. A new infantile case of alpha-N-acetylgalactosaminidase deficiency. Cardiomyopathy as a presenting symptom. J Inherit Metab Dis 30: 108.
  • Herrmann T, Schindler D, Tabe H, Onodera O, Igarashi S, Polack A, et al. 1998. Molecular cloning, structural organization, sequence, chromosomal assignment, and expression of the mouse alpha- N-acetylgalactosaminidase gene. Gene 211: 205-214.
  • Hershfield JR, Pattabiraman N, Madhavarao CN, Namboodiri MA, 2007. Mutational analysis of aspartoacylase: implications for Canavan disease. Brain Res 1148: 1-14.
  • Janson CG, Kolodny EH, Zeng BJ, Raghavan S, Pastores G, Torres P, et al. 2006. Mild-onset presentation of Canavan's disease associated with novel G212A point mutation in aspartoacylase gene. Ann Neurol 59: 428-431.
  • Kanekura T, Sakuraba H, Matsuzawa F, Aikawa S, Doi H, Hirabayashi Y, et al. 2005. Three-dimensional structural studies of alpha-N-acetylgalacto- saminidase (alpha-NAGA) in alpha-NAGA deficiency (Kanzaki disease): different gene mutations cause peculiar structural changes in alpha-NAGAs resulting in different substrate specificities and clinical phenotypes. J Dermatol Sci 37: 15-20.
  • Karpati M, Gazit E, Goldman B, Frisch A, Colombo R, Peleg L, 2004. Specific mutations in the HEXA gene among Iraqi Jewish Tay-Sachs disease carriers: dating of founder ancestor. Neurogenetics 5: 35-40.
  • Liu GY, Xiong YZ, 2007. Isolation, sequence analysis and expression profile of a novel porcine gene, NIP7, differentially expressed in the longissimus dorsi muscle tissues from Meishan, Meishan Large White cross and Large White pigs. Mol Biol Rep 344: 213-219.
  • Liu YG, Xiong YZ, Deng CY, Zuo B, Zhang JH, 2004. Comparison of gene expression patterns in longissimus dorsi of pigs between the high-parent heterosis cross combination LandraceLarge White and the mid-parent heterosis cross combination Large WhiteMeishan. Asian-Aust J Anim Sci 17: 1192-1196.
  • McGinniss MJ, Brown DH, Fulwiler A, Marten M, Lim-Steele JS, Kaback MM, 2002. Eight novel mutations in the HEXA gene. Genet Med 4: 158-161.
  • Miklyaeva EI, Dong W, Bureau A, Fattahie R, Xu Y, Su M, et al. 2004. Late onset Tay-Sachs disease in mice with targeted disruption of the Hexa gene: behavioral changes and pathology of the central nervous system. Brain Res 1001: 37-50.
  • Surendran S, Matalon KM, Tyring SK, Matalón R, 2003. Molecular basis of Canavan's disease: from human to mouse. J Child Neurol 18: 604-610.
  • Zeng BJ, Wang ZH, Ribeiro LA, Leone P, De Gasperi R, Kim SJ, et al. 2002. Identification and characterization of novel mutations of the aspartoacylase gene in non-Jewish patients with Canavan disease. J Inherit Metab Dis 25: 557-570.

Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

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