Genetic damage, or mutation, that occurs to these genes contributes to the development of a cancerous tumour.
Methylation-mediated silencing of genes contributes to docetaxel resistance in prostate cancer.
Aberrant regulation of miRNA genes contributes to pathogenesis of a wide range of human diseases, including cancer.
The absence of an increased burden of smaller CNVs in individuals with autism and the failure of most large hotspots to refine to single genes is consistent with a model where imbalance of multiple genes contributes to a disease state.
Salinity-induced down-regulation of most aquaporin transcripts has been observed in roots of salt-stressed Arabidopsis and maize plants (Maurel et al. [2008]), suggesting that a transcriptional regulation on aquaporin genes contributes to the L pr down-regulation under salinity stress.
In the networks consisting of four viral RNAs (pgRNA, pre-S, S, and X mRNAs) and four host mRNAs (cyclin G1, PBF, NT5C3, and Bcl-2), elevated expression of de-repressed host genes contributes to enhanced HBV replication, persistent viral infection, and HCC development.
One potential consequence of these CNVs is that normal regulation and expression of these genes contributes to the T1D disease process.
Whether altered transcription of these genes contributes to the change in hemolytic activity in Δstp1 and Δstk1 (Fig. 2) mutant strains has yet to be established.
While it is long believed that differential expression of neuroendocrine genes contributes to establishing seasonal reproductive rhythms, no systems-level investigation has yet been conducted.
Collectively, the data implicate that more than one gene is likely to be involved in the pathogenesis of MDS, and support the hypothesis that haploinsufficiency of multiple 5q31.2 genes contributes to MDS initiation or progression.
