Essay --

This paper aims to describe the role and function of protein Helicase.Helicases are enzymes that ingestion ATP-driven motor force to unwind double-stranded DNA or RNA (Wu, 2012). number 1 discover in E Coli in 1976 (Abdel-Monem et al, 1976) with the first eukaryotic helicase protein discovered soon after in 1978 (Hotta & Stern, 1978). Since these discoveries, many more confusable enzymes and proteins fall in been discovered. It breaks the hydrogen bonds organize between opposing strands of DNA with energy formed through the hydrolysis of ATP to ADP and inorganic phosphate (Hartsuiker, 2013). The separation of strands is necessity as newly formed strands need to be transcribed employ the nucleotide sequence of an open DNA strand. The protein is built around 6 sub-units which form an hexameric ring with assymetic symmetry.The biochemical properties of helicases are all very equal however, the presence of circumstantial motifs (short chains of DNA, primarily used for structure) alters which family of helicases they fall into, how that specific helicase will work and subsequently mutations in these specific motifs will progress to specific differences in protein synthesis. There are 4 Superfamilies created through note of 7 conserved motifs, roughly made from 300-500 amino acids(Hall & Matson, 2002). All helicases covered in this paper belong the largest family(Unmate et al, 2011) Super Family 2 (SF2) which are acknowledge by 9 conserved motifs. XPB and XPD are both DNA helicase structures, mutations in their helicase motifs can cause Xeroderma Pigmentosum (XP) and similar diseases. XPD and XPDs cellular functions involve nucleotide Excision Repair, which removes DNA damaged from UV rays. During Xeroderma Pigmentosum, these damaged stran... ..., similar to BLM, XPD, XPB, and WRN is found in Super family 2 and is a part of the DEAH package helicases. These helicases are involved in nuclear transcription and control of constituent expression (De La Cruz et al, 1999). Mutations to this gene coding protein can result in an individual suffering from ATR-X syndrome, causing psychomotor retardation, -thalassemia and the expression of abnormal phenotypes in both the genitals and face. A 2kb deletion mutation has been observed in the XH2 gene, removing both coding and non-coding sequences. This mutation results in the down-regulation of - globin, this irregular haemoglobins are produced which without delay results in - thalassemia (Gibbons et al, 1995). The mutated globin proteins have a lower chemical attraction with oxygen, thus less oxygen is in the blood, and less oxygen reaches the drumhead which can trigger psychomotor retardation.