Such deregulation of genes has been attributed, at least partially, to interactions and recruitments of several transcription factors to the mutant HTT aggregates. Transcription factors like TBP, CBP, p53, Sp1, NFkB and others are recruited to aggregates formed by mutant HTT, the hallmark of HD. Functional consequence of such recruitment remains Succinylsulfathiazole largely unknown. Recruitment of TFs to the aggregates may result in loss of functions of the TFs. This can explain the altered expressions of many genes in HD. In the presence of mutated HTT exon1, repression of transcription from p53responsive promoters is detected, indicating hypo function of p53 in HD. However, the level of p53 is increased in various models of HD as well as in the affected tissue in HD patients possibly due to post transcriptional or post-translational modifications. It has also been shown that p53 directly interacts with the promoter sequence of HTT gene that harbors multiple p53 response elements. Increased expression of mutant HTT due to higher level of p53 in turn may increase the aggregates formed by mutant HTT. Direct evidence that p53 participates in the pathogenesis of HD is also available. However, effects of recruitment and interaction of NFkB with mutant HTT in HD pathogenesis remains unclear. In a cell model of HD, it has been shown that NFkB activity is increased in the early stage when there are no visible aggregates of mutant HTT, while at a later stage when visible aggregates are formed, NFkB activity is reduced. Similar decrease in NFkB activity after 72 hours of Demethylzeylasteral induction of mutant HTT was also observed in a cell model of HD, while in early stage of induction, NFkB activity was increased. This dual role of mutant HTT on NFkB activity could be due to initial protective action of NFkB, which is suppressed at a later stage by the recruitment of NFkB into the aggregates. Alteration of NFkB activity may result in altered expression of NFkB regulated genes. Recent experiments show that at least in few specific cases, mature miRNA can alter the expression of genes even by binding to the coding regions as well as to the 59 UTRs of its targets. It thus provides further complex regulation of genes by miRNAs.