DNA-binding domain

which are members of a large super family of proteins that function as ligand-activated transcription factors (Katzenellenbogen and Katzenellenbogen, 1996). Both receptors have direct differentiative influences on reproductive organs and have similar binding affinity to estradiol (Kuiper et al., 1997; Drummond et al., 1999). Although, there are significant amino acid differences in the regions of these receptors that would be expected to influence transcriptional activity (Hall and McDonnell, 1999). More

of several functional domains: 1. An acidic N-terminus transcription-activating domain 1 and 2 (TAD1/2) - This region interacts with various transcription factors 2. Proline-rich region (PRR) - This plays a role in p53 stability 3. Central DNA binding domain (DBD) - required for binding to specific sites on the DNA. 4. Tetramerization domain (OD) - required for the assembly of the functional tetramer. 5. Carboxyl terminus domain (CTD) - which is bound to DNA binding domain and is involved in negative

genes are called oncogenes, where the DNA is altered from its original form. These gene help in growth regulation and division of the cells and are often causes the cells to divide out of control causing cancer to develop from the mutations of the gene p53. The p53 protein has five highly sustained regions within a cross species amino acid sequence which are also known as domains. Of these five, there are four functional domains, transcriptional activation domain at the N-terminus,

humans, three major types of DNA ligases are reported: DNA ligase I (hligI), DNA ligase III (hligIII) and DNA ligase IV (hligIV). hligI plays an important role in DNA replication by joining Okazaki fragments on the lagging strand of DNA. Apart from this it also plays important roles in DNA damage repair pathways, single strand breaks are repaired by nucleotide excision repair (NER) and base excision repair (BER) pathways. Results of preclinical studies support that Human DNA ligases are an attractive

suppressor p53). Another main role p53 plays is as a tumor suppressor and once activated, protects against cancer by “functioning as a sequence-specific transcription factor, through protein-protein interactions, activating cell cycle arrest, apoptosis, and DNA damage repair (Brachova).” As one

nuclease domains: HNH (39) and RuvC-like (40), within the Streptococcus pyogenes Cas9 (SpCas9) protein conduct the function of cleaving DNA strands. Studies have confirmed that the tracrRNA: crRNA duplex structure will lead to the sequence-specific DNA cleavage (41). PAM short sequence facilitates crRNA to recognize the targeted DNA sequence (42). Cas9 protein cuts the specific DNA strand that is complementary to the 20bp crRNA sequence via HNH domain; on the other hand, the SpCas9 RuvC-like domain cleaves

any process by which genetic material is changed in such a way as to make possible the production of new substances or new functions through the insertion or deletion of genes. This is achieved through the cleavage of DNA at a specific gene sequence, followed by the repair of the DNA by non-homologous end joining or homology directed repair (Zhang, Ferreira & Schnorrer, 2014). Consequently, if left alone double stranded breaks can lead to cell death, as a result cells have developed many

wild typed Top3β • Top3β-C666R lost 10 folds of mRNA binding capacity while Top3β-R472Q retain mRNA binding capacity comparing to Top3β-WT • Association with FMRP and Top3β-C666R and Top3β-R472Q is impaired but with TDRD3 they formed complex with 30% less amount comparing with Top3β-WT. • Top3β-C666R variant lacked its ability to rescue abnormal synaptic branches and boutons numbers at NKJs of Drosophila Discussion Top3β is the major mRNA binding topoisomerase in human cells. Top1, Top2α, Top2β,

have been many discoveries in the world of science such as; the structure of deoxyribonucleic acid (DNA) by Watson and Crick, the purines and pyrmides of DNA by the Human Genome Project, yet despite discovering genetic changes associated with Huntington’s disease, Alzheimer's Disease, and thousands of other diseases with deleterious genetic mutations, The process of openly altering the structure of DNA and using it in many industries from agriculture to clinical research has only just began. Gene targeting

and it will bind to both receptors and JAK in order to turn off the signaling pathway. The last type is PIAS proteins and it has a structure of Zinc binding domain in center, a carboxyl domain, and preserved SAP domain located at terminus-N, which related to binding process. PIAS protein binds to phosphorylated STAT dimer and prevents it from binding with