Anti-IL12A polyclonal antibody [Biotin]

GWAS studies have identified variant rs 17810546 in a non-coding region on chromosome 3 as a risk factor for several auto-immune diseases, including Celiac Disease. In silico analysis reveals that this variant is located in a transcription regulatory site. By means of reporter constructs we show that this region can override the expression rate of a gene as determined by its native promoter and that this modulation is influenced by the genetic composition of the haplotype which rs17810546 forms with a nearby other variant, rs761008. Secondly, we present data that this genetically imprinted modulation could be involved in Celiac Disease through the IL12A gene which is located 40 Kb downstream of this regulatory region. Based on our findings it is most likely that the IL12A gene does so as part of the cytokine IL-35.

Comparative mapping of Ateles paniscus chamek and man indicated that four human 3p markers are syntenic in this karyotypically rearranged neotropical primate. The evolutionary conservation of this gene cluster includes three adjacent human shortest regions of overlap (SROs): 3p21.1 (ACY1), 3p21.3-->p21.2 (CACNA1D), and 3p21.3 (ZNF64). A fourth syntenic marker (ATP2B2), at a more distal human SRO (3p26-->p25), indicated that human 3pter-->p14 is evolutionarily conserved in Ateles chromosome 3 (APC 3). Conversely, allocations of two human 3q markers (AGTR1 and IL12A) clearly excluded APC 3. Finally, allocation of the major histocompatibility complex class I genes further confirmed human 6p-6q dissociations Ateles.