Nucleophosmin

Which of the following is NOT a key factor in determining if a cell will be reversibly or

This assignment is aimed to enable me identify an unknown sequence that has been provided. I have thereby used the DNA database, journals on cell division and medical publications in undertaking this assignment. To identify the sequence, application of theories and practical modelling is necessary for this kind of work. The sequence to be analysed is essentially the nucleotides present in cells sample under examination. Since each of the four typical nucleotides are available, chain extension continues typically until, by chance, DNA polymerase embeds a dideoxy- nucleotide which is indicated as hued letters rather than the ordinary de-oxynucleotide demonstrated as vertical lines. In the event that the proportion of typical nucleotide to the dideoxy forms is sufficiently high, some DNA strands will succeed in including a few hundred nucleotides before insertion of the dideoxy form stops the methodology.

Three types of reaction were conducted, unimolecular nucleophilic substitution reaction (SN1), unimolecular elimination reaction (E1), and bimolecular nucleophilic substitution reaction (SN2). Substitution and elimination reactions are important to allow for the transformation of reactants to desired product. This is extremely important when it comes to synthesis of different molecules for research, commercial, and medical purposes. SN1reaction was to create 2-chloro-2-methylbutane from 2-methyl-2-butanol with a reaction yield of 2.28 g (21.4 mmol) and the reaction product was analyzed by infrared spectroscopy (IR) to determine the purity of 2-chloro-2-mehtlybutane. E1 was to create cyclohexene from cyclohexanol with a reaction yield of 0.17

Cancer known in medicine as a malignant neoplasm is one of the biggest killers worldwide. In 2007, cancer caused roughly 13% (7.9 million) of the planet’s deaths (Jemal, 2011). This will more greatly affect an aging society such as ours in years to come, and yet it is already the foremost cause of death in the developed world. The main reason cancer causes so many fatalities the body’s inability to mount an effective response to the failure of DNA replication within the body. This results in a mass

Apart from PTMs of the H3 nucleosomes, the centromere code is also unique because CENP-A nucleosomes also undergo PTMs and regulate centromere function (Figure 1). The centromeric histone H4 of CENP-A containing nucleosomes undergo monomethylation at Lysine 20 following deposition of CENP-A into centromeres[94, 95]. When present in the H3 nucleosome, H4K20me1 is associated with transcribed regions throughout the genome[96]. Targeting the H4K20me1-specific demethylase PHF8 to centromeres reduces centromeric level of H4K20me1 and results in reduced recruitment of CENPT and CENP-H[94]. It is not yet clear whether this conserved H4K20me1 is directly responsible for the recruitment of the kinetochore components, or if it is an indirect effect caused by reduced

The assessment of the location in the cytoplasm of p16 is a pretty new occurrence. Presently, expression of p16 in the cytoplasm has been thought of as background information in much research. Those results should be looked at with carefulness (41). Many propositions to elucidate the existence of p16 in the cytoplasm have been explained. It appears as though accumulation in the cytoplasm is not linked to a modification of the p16 gene (15). Phosphorylation of p16 leads to the creation of the p16/CDK4 complex. This stops binding cyclin D and

During prophase the spindle fibers are developed and moving towards opposite poles. During metaphase the chromatids aligns at the plane of the cell equator. During anaphase, the paired sister chromatids are separated and each move towards one pole, at this point the cohesin at the centromere are removed. Cohesin, a protein complex, plays an essential role during this process. The core subunits of the cohesin complex are: Smc 1 and 3 (structural maintenance of chromosome (5)), Rad21, and Scc 2-4 (adherin factor) which form a ring-like structure that performs cohesion on the sister chromatids in S phase and is maintained until metaphase (4). The Smc proteins contain ATPase (ABC type) at the terminal domains separated by a coiled coil domains and hinge domains which allows for interaction between the N- and C-terminals which are bridge by a heterodimer (Rad21 and Scc3 complex) (1). Cohesion process requires the Smc proteins to have the hinge domain, and ATPase activity in order for cohesin to associate with chromatin during the G1-phase (1,4). The Scc2-4 complex is required to load the cohesin complex onto chromatin (6). Scc complexes are used to mediate protein-protein interactions essential for cell division. Depletion in the protein results in severe premature sister chromatid separation (PCS) that will be discussed later (7). Once cohesion is established, Pds5 complex serves to maintain the sister chromatid structure through the G2-phase

Eukaryotic cells contain a sphere-shaped nucleus that protects the genetic information (DNA) and separates it from the cytoplasm. The nucleus itself is protected by a double membrane called, the nuclear envelope. The nuclear envelope is made up of nuclear membranes, nuclear lamina, and nuclear pore complexes. The nuclear lamina is the sturdy protein that gives the nucleus its structure and shape. As well as providing structural support, “the nuclear lamina is required for most nuclear activities, such as chromatin organization, DNA replication, cell cycle regulation, nuclear positioning within the cell, assembly/disassembly of the nucleus during cell division, as well as for modulating master regulatory genes and signaling pathways.” (Baek, McKenna, Eriksson; 2013) The ability of the cell to

DNA is tightly coiled around core histone proteins in chromatin, forming nucleosomes. Linker histones bind nucleosomes together as chromatin. Acetylation, Methylation, phosphorylation, or ubiquitination of the N-terminal tails of each of the core histones affect the binding of the histone proteins to DNA. These modifications change the structure of the chromatin and allowing transcription factors accessibility to DNA regions. The combined effect of these modifications creates a histone code, which regulates gene expression. Of these various modifications, histone acetylation is the extensively studied, because of its role in the development and progression of tumors. Histone acetylation is controlled by histone acetyltransferases (HATs) and

P53 is a tumor suppressor gene. In all kinds of malignant tumors, above 50% appears p53 gene mutation. The protein encoded by this gene is a transcriptional factor, which controls to start the cell cycle. Many signals of the cell health directly send to the p53 protein. It also decides when the cells begin the division. If the cells are damaged and cannot be repaired, the p53 protein would start the boot process and lead the cell go to apoptosis died. Some p53 deficient cells without this control, under adverse conditions, cells will continue to split. Just like any other tumor suppressor, p53 gene normally plays the role of slowing down or monitoring the cell division. The Inhibiting cancer genes “p53” in cells judges the extent of DNA damage.

Nucleosomes are made of DNA wrapped around eight histone proteins and they are called a histone octamer. Each histone octamer has two copies of the histone proteins H2A, H2B, H3, and H4. The chain of nucleosomes is then wrapped into a 30 nm spiral called a solenoid, where additional H1 histone proteins are associated with each nucleosome to maintain the chromosome structure.

Chromosomal instability is a central feature of many tumours and is present in about 85% of colorectal tumours. It is characterised predominantly by frequent chromosomal abnormalities which include translocations, gains, and losses of entire chromosomes or their segments [Grady, 2004; Baba, 2009]. Although the causes of chromosomal instability are still poorly understood it is thought to arise as a result of mutation and amplification of a number of genes including Aurora-A, encoding a serine-threonine kinase. This enzyme is an important regulatory protein involved in mitotic entry, bipolar spindle morphology, centrosome maturation and segregation and regulation of the G2-M transition during mitosis [Berdnik and Knoblich, 2002; Hirota et. al, 2003; Fu et. al, 2007; Sen et. al, 2008]. Activation of Aurora-A in experimental systems often confers malignant phenotype by inducing the formation of a multipolar bipolar spindle which results in multinucleation concomitant with numerical centrosome aberrations [Meraldi et. al, 2002; Anand et. al, 2003]. A study by Zhou et. al [1998] showed that transiently transfecting an Aurora-A expression construct into near diploid human breast epithelial cell lines induced aneuploidy and thus suggested that specific gene abnormalities can directly influence chromosome ploidy in tumour cells. Furthermore, a group led by Wang et. al [2006] showed transgenic mice over-expressing Aurora-A in mammary epithelium caused neoplasmic transformation

The function of a nucleus includes holding the DNA and RNA for the cell. The RNA plays an important role in making proteins. The RNA also configures amino acids into special proteins for the cell to use. The nucleus also makes exact copies of it’s DNA

The decision of NSCs to either stay in the pool of proliferating, undifferentiated cells or to differentiate is dictated by extracellular and intracellular factors that are affected by the cell cycle mechanism.

3) The last conclusion was, the size of the cells interfere with the size of nucleolus.2