The reason these genes produce an increase in risk of coeliac disease is that the receptors formed by these genes bind to gliadin peptides more tightly than other forms of the antigen-presenting receptor.
Proteins from these genes bind to small guide RNAs to form TE silencing complexes [ 42, 43].
SOX genes bind to the minor groove in DNA to control diverse developmental processes [ 3].
The protein products of the TSC1 (hamartin) and TSC2 (tuberin) genes bind to each other and function together to modulate downstream signaling pathways.
R2R3 MYB genes tend to display limited homology (aside from the highly conserved DNA binding region), and the code by which R2R3 MYB genes bind to specific sequences has not been well elucidated [ 45, 48].
These pro-survival genes bind to beclin 1, and form a trimeric complex, which inhibits beclin 1-mediated autophagy function, resulting in proliferation and survival of cancer cells (Furuya et al, 2005; Pattingre et al, 2005).
The last two genes, namely ERF4 and ERF9, which are the members of the ERF/AP2 transcription factor family, are involved in various reactions to abiotic stresses [ 66]; these two genes bind to the GCC box, DRE/CRT, CE1 elements, and they acted as repressors of gene transcription, enhancing plant tolerance to multiple stresses [ 67].
The three RUNX genes bind to the same DNA motif and modify the expression of target genes through recruitment of transcriptional modulators, which are also shared [ 30]; functional differences between the three RUNX genes are attained by way of tightly regulated spatiotemporal expression patterns.
For example, all three of the skeletal muscle-associated myomesin genes showed downregulation in FSHD vs. control myotubes of about 4 to 9 fold, and the products of these genes bind to other muscle structural proteins in a dose-dependent manner as major components of the myofibrillar M-band.
