SOD1

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  • Mutant SOD1 And Pro-Apoptotic

    Some experiments were aimed at finding how SOD1 becomes pro-apoptotic (promoting programmed cell death) due to the fact that healthy SOD1 are against programmed cell death (Pasinelli et al. 2004). The pro-apoptotic characteristic of mutant SOD1 is demonstrated in vivo and in vitro. The mitochondria inside cells firmly control apoptosis, and the mutant SOD1 that aggregates inside mitochondria triggers the programmed cell death of motor neurons (Pasinelli et al. 2004). One experiment studied proteins that interact with mutant SOD1, specifically Bcl-2 which is anti-apoptotic, in order to explain the apoptotic nature of mutant SOD1 (Pasinelli et al. 2004). The methods that were used involve in vitro approaches and Western blot analysis. The outcomes were that mutant SOD1 and Bcl-2 interact with each other in vivo in the spinal cord, and they both together are pro-apoptotic (Pasinelli et al. 2004). In other words, Bcl-2 was an anti-apoptotic protein when standing alone, and when it directly interacted with mutant SOD1, the protein and the gene convert to pro-apoptosis, or in support of cell death; this could be due to a conformational change in Bcl-2.…

    Words: 960 - Pages: 4
  • Causes Of Motor Neure Disease

    The C90RF72 gene however, creates a protein located in the brain that has an unusual relationship with neurons as it is often found around the cytoplasm of those specific cells. Similar to the SOD1 gene, if a mutation arises the protein will no longer operate efficiently leading to a malfunction within the neuron cells and is highly considered to be the prime reason for the genetic disorder. Despite the effects and causes of MND it can be clearly said that the disease is increasing in terms of…

    Words: 1266 - Pages: 6
  • Alkylated Polycyclic Aromatic Cells: The Effects Of PAH?

    cell permeant, positively-charged, red-orange lipophilic cationic dye, and stain specifically polarized mitochondria rather than other intracellular organelles (Cottet-Rousselle et al. 2011). The amount of TMRE uptake by mitochondria is directly proportional to MMP and can be visualized by the levels of fluorescence at 579 nm/599 nm (Ex/Em). Depolarized or inactive mitochondria have decreased membrane potential and fail to sequester TMRE. Significant dose dependent decreases in TMRE fluorescence…

    Words: 934 - Pages: 4
  • Amyotrophic Lateral Sclerosis Case Study

    causes multisystem progressive debilitation that leads to muscular failure and eventual death. (Orsini, 2015) According to research from 2007, ALS was thought to be totally sporadic deriving from multiple mutated genes in congruence with environmental attributes with an emphasis on military members and Italian soccer players. (Commare, 2007) Since that time, several research studies have been conducted in order to delve into the causative factors of ALS in order to properly combat this disease.…

    Words: 1157 - Pages: 5
  • Statement Of Purpose: Biomedical Engineering

    biochemical knowledge into practical research, I aimed to examine therapeutics for incurable diseases. During past three years, I have had the chance to study in vivo effects of “Molecular Tweezers” (MTs) as novel therapeutic agents on neurodegenerative diseases. MTs are synthetic small molecules that bind to lysine residues on amyloidogenic proteins, reducing their aggregation and toxicity. Utilizing various biochemical techniques such as protein extraction, immunoblotting, and dot blotting, I…

    Words: 1453 - Pages: 6
  • Irish Terrier Essay

    fiber protein. Male puppies 6-10 weeks of age usually present with difficulty swallowing followed by a stiff neck and stilted gait. There is muscle atrophy but the tongue and hamstring muscles become more developed. A hereditary myopathy similar to that seen in Labrador Retrievers has been reported in Irish terriers. 5, 7 A deficiency in type II muscle fibers can cause stiffness and megaesophagus in dogs less than six months of age. NEUROLOGIC Degenerative myelopathy (DM), similar to…

    Words: 1811 - Pages: 8
  • What Are Ubiquitin Conjugating Partners Of CHIP?

    into different boxes according to their degradative pathways. Yellow boxes represent substrates, which are degraded by the proteasome, whereas brown boxes represent the lysosomal degradation of CHIP substrates. Substrates degraded by both proteasomal and lysosomal pathways are shown in the green box. CHIP also ubiquitinates few of its substrates to functionally regulate them instead of degrading, shown within the purple box. 5. CHIP, a major E3 ubiquitin ligase of neurodegenerative disorders:…

    Words: 1627 - Pages: 7
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