High impact information on Cxxc6

• Demonstration of a testis-specific trans-acting factor Tet-1 in vitro that binds to the promoter of the mouse protamine 1 gene [1].
• DNase I footprinting demonstrated the presence of a DNA-binding factor around position -60 (Tet-1) in testis nuclear extracts, but not in other tissues [1].
• Since mutational analysis in transcriptional and binding assays demonstrates that the Tet-1 site is responsible for transcriptional activation, we suggest that Tet-1 is a novel tissue-specific trans-acting factor [1].
• Although the first 8-mer in the Tet-1 11-mer shares homology with the cyclic AMP-responsive element, Tet-1 is demonstrated to be distinct from known cAMP-responsive element-binding factors [1].
• In vivo, the accidental loss of insulator flanks during transgene insertion in one transgenic NOD founder, tet1, re-established leakiness with high level, exclusive ICA69-transgene expression in stromal elements of thymus and spleen [2].

Anatomical context of Cxxc6

• Deviation of T cell autoreactivity from major to cryptic target epitopes in tet1 mice provides a fortuitous model to explain previously observed diabetes protection by immunotherapy or autoantigen transgenes despite apparent failure to achieve tolerance to the full length islet antigens [2].

Other interactions of Cxxc6

• The relevance of this conserved element in the expression of P1 genes is strongly supported by the recent demonstration of a mouse testis trans-acting factor [Tet-1; Tamura et al., J. Biol. Chem. 267 (1992) 4327-4332] which binds and matches in the mouse the first 11 bp of the corresponding consensus Prot1C sequence reported here [3].

Analytical, diagnostic and therapeutic context of Cxxc6

• Gel shift analysis also revealed the presence of testis-specific Tet-1 [1].

References