Another explanation could be that Chloroquine Phosphate TcSub2 is related to transcription of specific mRNAs as consequence of its role in regulation of gene expression. To further investigate the function of TcSub2, we attempted to knockout the TcSub2 gene to obtain phenotypic Chlorhexidine hydrochloride alterations related to mRNA export. However, the null knockout lineages of T. cruzi were not viable. Studies show that it is an essential protein in other eukaryotes because the knockdown of Sub2 homologs inhibits cell growth. Unfortunately, knockout of a single TcSub2 allele was not enough to affect morphology and cell growth. Although the single-allele TcSub2 knockouts had around 50% less TcSub2 protein, this did not alter mRNA export. It is therefore necessary to apply a regulated system to completely silence TcSub2 expression to get more information regarding to its function in T. cruzi. The absence of approaches of inducible silencing, such as RNA interference, in T. cruzi preclude suitable studies for this. On the other hand, T. bruceii is a suitable model to study essential genes using inducible system based on RNAi in trypanosomes. Taking in account that Sub2 is highly conserved in trypanosomes, we decided to use T. bruceii to study the function of this protein. The data obtained demonstrated that it is really an essential protein since its knockdown inhibits the cellular growth. Similar to other eukaryotes, the silencing of TbSub2 expression caused 
translation inhibition and robust accumulation of bulk polyadenylated mRNAs in the nucleoplasm. These phenotypes are also observed when the expression of homologs is silenced in metazoan.Interestingly, we also observed an arrest of cell cycle in G2 phase, mainly after 72 hours of RNAi induction when the level of the proteins was reduced by 70%. In the same way, knockdown of UAP56, the homolog in humans, resulted in mitotic defects. Taking together, the trypanosome protein has similar characteristics to its orthologs in higher eukaryotes, possibly reflecting a similar function in these parasites. In the context of nuclear mRNA metabolism in trypanosomatids, nucleocytoplasmic transport is not well understood and data in this area will lend further insights into regulation of gene expression in these parasites. Herein, we identified a novel trypanosome protein that it is related to nuclear mRNA metabolism and proposed that the Tryp-Sub2 is a component of mRNA transcription/export pathway in these parasites. Whereas approximately half of CLL patients have an indolent clinical course that does not require treatment for many years, a more aggressive clinical course that necessitates treatment within a few years is diagnosed for the other half. These differences in clinical course correlate with molecular markers, including the mutational status of the surface immunoglobulins and the expression of intracellular tyrosine kinase ZAP-70. Despite a typically lower expression of CD20 compared to normal B cells, the combination of fludarabine and cyclophosphamide with the chimeric mouse/human anti-CD20 IgG1 monoclonal antibody rituximab has become standard first-line treatment that was approved by the Food and Drug Administration in 2010. In addition, alemtuzumab, a humanized anti-CD52 IgG1 mAb, was FDA-approved in 2001 as single agent for CLL therapy. Alemtuzumab is frequently used for second-line treatment, but is ineffective in CLL patients with bulky lymphadenopathy. In 2009, fully human IgG1 mAb ofatumumab, which binds to a CD20 epitope different from rituximab, was FDA-approved for treating CLL patients refractory to fludarabine and alemtuzumab.