Dna Synthesis Case Study

Adrienne Livioco August 24, 2017 MDA110 - Pharmacology DNA Recombinant and How it Helps Certain Companies Produce Certain Drugs Technology has flourished and has improved our way of living in many ways than one. In the medical world, it has definitely shaped our ways to helping patients through medication. For instance, diabetes, or growth and clotting disorders among the spectrum of human diseases related to protein absence or malfunction. A lot of the medications that we use today are created from bacteria, yeast, insect cells, and mammalian cells, which boost the production of the protein within the human body. For example, insulin is a very in demand medication due to the increase of diabetes as a disease. Before technology, insulin would

1. Explain how an acid and a base are distinguished and how the pH scale operates as a logarithmic function. An acid and base are distinguished by the negative hydrogen concentration in a substance. If a substances loses its hydrogen concentration, it is more acidic. If a substance accepts more hydrogen, it

In the context of the cell cycle, P53 is shown to have a G1 and G2/M checkpoint function [23]; in fact, upon receiving a stimulus such as DNA damage, p53 induces cell cycle arrest providing time for the cell to repair the genomic damage before being released back into the proliferating pool . The best known P53 target gene product involved in this process is the cyclin-dependent kinase (CDK) inhibitor p21 [18]. The progression through the S phase of the cell cycle is tightly controlled by CDKs [19]. P21 functions by inhibiting Cyclin-CDK complexes, therefore, hindering the cell cycle transition from G1 to S phase [23]. In addition to being implicated in the G1/S arrest of the cell cycle, it has been demonstrated that P21, alongside p53, is also essential in the G2/M phase [23,

While CDK- cyclin complexes guide the cell through a defined sequence of events, the cells have evolved surveillance mechanisms ( or checkpoints) that are set at various stages of the cell cycle. These checkpoints can sense possible defects during DNA synthesis and chromosome segregation and halt the cell cycle through modulating of CDK-cyclin activity if the conditions for successful cell division are not met. This allows cells to properly repair those defects, thus preventing their transmission to the resulting daughter cells.

In the SOS response, preset enzymes by SOS regulon genes initiate recombination repair once notified of DNA damage. These genes, among which are umuC and umuD, code for several DNA polymerases. LexA will regularly repress SOS genes to prohibit unwanted transcription from occurring if DNA is injured. From this event, RecA is beckoned through signaling to knock out LexA, thereby alleviating the proteins and increasing umuC and umuD levels. The two fragmented proteins then act as elongation factors to interact with stalled DNA polymerase and resume synthesize past a lesion. RecA will stimulate autocatalytic cleavage by forming a complex with LexA, though it is not completely known how such formation can lead to cleavage (5). The filament then binds to and activates LexA to cleave other bound proteins, thus stimulating DNA

DNA is used to make polypeptides by having the DNA copied into mRNA. mRNA is pretty much a replication of DNA, making one strand instead of two. Then the mRNA fits into the pores, or tiny holes of the endoplasmic and reticulum. Then it forms into a protein, folding itself to get out of the cell and going out into the rest of the body. there are things called codons and anti-codons that relate to this process. Codons are 3 nitrogen bases that make up one amino acid, and anticodons are a part of the process called transcription. Transcription is when mRNA copies the sequence of the bases in an amino acid. Ribosomes help this process ouot, in which they set up a certain destination for which the DNA can be copied. However, translation is a process

Werner syndrome is an autosomal recessive genetic condition associated with the WRN gene (7). The WRN gene found on chromosome 8 encodes a protein called Werner (4). The Werner protein works as a helicase assisting in the unwinding of DNA. The helicase belongs to the RecQ helicase family and assists in DNA repair, maintenance and regulation of telomeres (4). The Werner protein also functions as an exonuclease that also assists in DNA repair, replication and transcription (4). The Werner protein has been found to be essential in repairing double stranded breaks during replication fork stalling (3). The WRN gene and Werner protein demonstrate an essential role in the integrity and stability of DNA.

Nonetheless we observed two distinct features connected with the core consensus sequence of Epsilonproteobacterial DnaA boxes and DnaA-DnaA box interactions: strict conservation of thymine at the 5th position and the binding of Epsilonproteobacterial DnaA to guanine G4 of a DnaA box. So far the 5th positions of the E. coli consensus DnaA box (TTWTNCACA) and the M. tuberculosis DnaA box (YWRTCCACA) were considered to be variable without influencing affinity towards cognate DnaAs (Fujikawa et al., 2003; Schaper and Messer, 1995; Tsodikov and Biswas, 2011). However, it should be noted that in both species, the 5th position of DnaA box is preferentially occupied by the C residue. All other bases of the sequence, either of the upper or the lower strand, interact with DnaA, and any deviation from the most stringent TTATNCACA consensus sequence results in reduced DnaA affinity towards the less perfect boxes.

DNA Double Strand Breaks (DSBs) are valuable when controlled, but potentially fatal when not – the programmed DSB is an essential part of particular cellular processes (e.g. VDJ switch recombination during immune system development and during homologous recombination in meiosis and mitosis), but an unprogrammed DSB is also considered the

Cancer, also known as a malignant tumor, is a disease in which some cells in the body multiply uncontrollably leading to a mass of abnormal cells (“What is Cancer”).This is the result of damage to the DNA (deoxyribonucleic acid) of a normal healthy cell which causes the natural biological function of the cell behavior to become altered (Mandal). Normal cell behavior is directed by the DNA which regulates the growth and death of the cell among other things (Mandal). When a normal cell’s DNA is damaged, the cell tries to repair the DNA and if it is unable to

DNA repair in motion: The mechanical basis of transcription-coupled repair in prokaryotes Proper gene expression is crucial for normal physiological development. Unfortunately, the structural and functional integrity of cellular DNA is constantly at risk by intrinsic and extrinsic factors, from mistakes in metabolic processes to radiation damage. DNA repair pathways are critical processes that address these offenses by maintaining the level genomic integrity necessary for accurate cellular division and function. These pathways involve the seamless integration of repair with processes that operate on DNA, such as replication and transcription [1]. However, the coordination of these various pathways in DNA repair and the mechanisms by which specific sites of damage are recognized remain poorly characterized.

In cells, DNA is replicated from chromosomes with two points of regulation: a six protein complex forms at an origin and is activated by proteins that can modify others (Gambus et al, 2006; Labib, 2010; Zegerman and Diffley, 2006). This draws more proteins towards the origin for initiation to occur. Origins are specific DNA sequences where the two DNA strands are unwound for replication, creating fork-like structures (Labib, 2010). Origin unwinding occurs by the six protein complex mentioned with other initiator proteins and a four protein complex called GINS (Gambus et al, 2006). Another six protein complex called the Origin Recognition Complex orders these components at the origin (Takeda et al, 2005). DNA replication is then carried

In 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 target for the development of new anticancer agents for selective inhibition against rapidly proliferating cancer cells. In this mini-review, we will provide a brief discourse of the recently reported human DNA ligase inhibitors as

The Process of DNA Replication   The process of DNA replication plays a crucial role in providing genetic continuity from one generation to the next. Knowledge of the structure of DNA began with the discovery of nucleic acids in 1869. In 1952, an accurate model of

Answer: Nucleotide Excision Repair: This mechanism can repair the large change caused by the damage in the double helix of the DNA. The damage in the DNA is screened by the multienzyme complex, these set of enzymes scrutinizes for any kind of lesions that may appear on the double helix. These changes on the double helix are listed as; 1) Covalent Interaction of large hydrocarbons with DNA bases (such as carcinogenic molecules found in the toxic substances like smoke, tar etc.), 2) Dimers caused by the UV light from sun which causes pairing of pyrimidine bases, such as, T-T, T-C, and C-C.