Primers for amplifying major histocompatibility complex class II DQB and DRB exon 2 in the Australian sea lion (Neophoca cinerea)

2014 ◽  
Vol 6 (4) ◽  
pp. 813-816 ◽  
Author(s):  
Q. Lau ◽  
T. Wilkin ◽  
E. Payne ◽  
R. Gray ◽  
J. Gongora ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Class Ii ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Sea Lion ◽  
Exon 2 ◽  
Neophoca Cinerea ◽  
Australian Sea Lion ◽  
Histocompatibility Complex

Genetic Diversity in Exon 2 of the Major Histocompatibility Complex Class II DQB1 Locus in Nigerian Goats

2013 ◽  
Vol 51 (11-12) ◽  
pp. 954-966 ◽  
Author(s):  
Abdulmojeed Yakubu ◽  
Adebowale E. Salako ◽  
Marcos De Donato ◽  
Michael I. Takeet ◽  
Sunday O. Peters ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Class Ii ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Exon 2 ◽  
Histocompatibility Complex

scholarly journals An Alternative Promoter in the Mouse Major Histocompatibility Complex Class II I-Aβ Gene: Implications for the Origin of CpG Islands

1998 ◽  
Vol 18 (8) ◽  
pp. 4433-4443 ◽  
Author(s):  
Donald Macleod ◽  
Robin R. Ali ◽  
Adrian Bird
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Cpg Island ◽  
Cpg Islands ◽  
Class Ii ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Exon 2 ◽  
Mouse Major Histocompatibility Complex ◽  
Histocompatibility Complex

ABSTRACT Nonmethylated CpG islands are generally located at the 5′ ends of genes, but a CpG island in the mouse major histocompatibility complex class II I-Aβ gene is remote from the promoter and covers exon 2. We have found that this CpG island includes a novel intronic promoter that is active in embryonic and germ cells. The resulting transcript potentially encodes a severely truncated protein which would lack the signal peptide and external β1 domains. The functional significance of the internal CpG island may be to facilitate gene conversion, thereby sustaining the high level of polymorphism seen at exon 2. Deletions of the I-Aβ CpG island promoter reduce transcription and frequently lead to methylation of the CpG island in a transgenic mouse assay. These and other results support the idea that all CpG islands arise at promoters that are active in early embryonic cells.

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