ok so if we have a given that zinc regulates expression of certain genes, how far are we towards having a list? a few more abstracts...
A role for zinc in gene expression (1983) !!!
"Zinc deficiency in Euglena gracilis has been shown to affect growth, morphology, cell cycle and mitosis. These observations are best explained by a role for zinc in gene regulation possibly through zinc dependent enzymes. A similar role for zinc in man may exist with genetic and medical implications."
Regulation of Intestinal Gene Expression by Dietary Zinc: Induction of Uroguanylin mRNA by Zinc Deficiency (2000)
http://jn.nutrition.org/content/130/5/1393S.full"The regulation of gene expression by nutrients plays an important role in the overall manifestations of nutritional deficiencies. Insufficient intakes of dietary micronutrients, such as zinc, produce profound effects in multiple organs and tissues. One of the major challenges, however, is to identify genes affected by changes in nutritional status."
A global view of the selectivity of zinc deprivation and excess on genes expressed in human THP-1 mononuclear cells (2003)
http://www.ncbi.nlm.nih.gov/pubmed/12756304"Microarrays composed of approximately 22,000 elements were used to identify those genes responsive to either zinc depletion, zinc supplementation, or both conditions. Hierarchal clustering and ANOVA revealed that approximately 5% or
1,045 genes were zinc responsive. Further sorting based on this pattern of the zinc responsiveness of these genes into seven groups revealed that
104 genes were linearly zinc responsive in a positive mode (i.e., increased expression as cellular zinc increases) and 86 genes that were linearly zinc responsive in a negative mode (i.e., decreased expression as cellular zinc increases). Expression of some genes was responsive to only zinc depletion or supplementation."Nutrient-gene interactions: a single nutrient and hundreds of target genes (2004)
http://www.ncbi.nlm.nih.gov/pubmed/15318805"Zinc deficiency caused pleiotropic alterations in mRNA/protein levels of hundreds of genes"
Evidence for reprogramming global gene expression during zinc deficiency in the HUT-78 cell line (2006)
http://www.ncbi.nlm.nih.gov/pubmed/16979875"gene expression for molecules that would increase T-lymphocyte response to signals from myeloid cells such as cytokine receptors and selected adhesion molecules were upregulated, whereas those associated with T-lymphocyte-directed immune functions, interleukin-2 and interleukin-6 receptors, the cytokine interleukin-4, and zinc finger transcription factors were downregulated"
Mechanisms of mammalian zinc-regulated gene expression (2008)
http://www.ncbi.nlm.nih.gov/pubmed/19021537"evidence for the involvement of zinc dyshomoeostasis in the aetiology of diseases, including Type 2 diabetes, Alzheimer's disease and cancer, highlights the importance of zinc-regulated gene expression"
arg i need a translation on this one. i recognize all the words, just not how they are put together

all i get is, MS, genes, predict outcome, related to zinc:
Zinc-ion binding and cytokine activity regulation pathways predicts outcome in relapsing–remitting multiple sclerosis (2007)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1941964/ "Using complementary-DNA microarrays we studied peripheral-blood gene expression patterns in 53 relapsing–remitting MS patients... An optimal set of 29 genes was depicted as a clinical outcome predictive gene expression signature and classified appropriately 88·9% of patients. This predictive signature was enriched by genes related biologically to zinc-ion binding and cytokine activity regulation pathways involved in inflammation and apoptosis...
Biological regulation of the predictive clinical outcome gene expression signature
Functional annotation of the 34 predictive genes demonstrated that this group of genes was enriched significantly by zinc-ion binding protein genes (S100B, KLF4, CAII) and by genes with cytokine activity (CCL17, MUC4, PTN VEGFB), P = 0·02 and P = 0·005, respectively (Fig. 3b). The Genomica software confirmed enrichment by the zinc-ion binding gene family and by cytokine activity genes using all the 431 differentiating gene expression signature data (Fig. 3c). Using these enriched gene-families, regulatory pathways were reconstructed (Fig. 3d,e). These pathways suggest that apoptosis regulation through zinc-ion binding and cytokine activity is responsible for Th1/Th2 shift and may play a role in the clinical outcome of RRMS."