Potential Therapy For Human Inflammatory Disorders

Proteins are the basis of the protoplasm (fluid living content of the cell that contains the cytoplasm and cell nucleus) and are found in all living organisms. Proteins make up the bulk of animals body’s non-skeletal structure. As enzymes, they catalyze biochemical reactions; as antibodies, they prevent the effects of invading organisms; and as hormones, they control metabolic processes (C. Bissonnette, 2011). The Biuret test was used to detect the presence of peptide bonds within proteins, and they were found present in test tube #9 (control for peptide bonds).

5. Explain why proteases are secreted in an inactive state and describe the means by which proteases are activated in the stomach and small intestine. – The enzymes protease, amylase and lipase, are potent enzymes that are capable of digesting the pancreatic cells- a process called autodigestion. To protect themselves from autodigestion in case the digestive enzymes accidentally get turned on, pancreatic cells produce enzymes in inactive form called zymogens, which are stored in membrane-bound sacks called zymogen granules. Enteropeptidase (also called enterokinase) is an enzyme produced by cells of the duodenum

Step 3: What protein will be your drug target? What property of that protein will you target? Design an assay/approach to identify an antidote for “degron”. (4 pts.)

Since gut inflammation of Crohn’s disease is characterized by abnormal decreases in the activity of the immunosuppressive cytokine transforming growth factor (TGF)–β1, which is induced by the increased level of SMAD7 protein, because it would prevent TGF-β1–associated and SMAD-associated signaling.[1] The formulation of Mongersen (formerly GED-0301) contains a 21-base single-strand phosphorothioate oligonucleotide, which would hybridize to the human SMAD7 messenger RNA (mRNA) complementary and then facilitate RNase H–mediated RNA degradation[1], thus it would reduce the translation product and help maintain the level of SMAD7 protein in the normal range.

(APP). APP is cleaved by two different enzymes to produce one amyloid beta monomer, which aggregates with other monomers to form cytotoxic

Tumour necrosis factor (TNF) is responsible for the disruption of the tight junction between endothelial cells which results in an increased permeability to plasma proteins and fluid, which worsens fluid accumulation in the alveoli further impairing gas exchanged (Bersten & Soni, 2009:709). TNF comprises of two different molecules, firstly TNFa which leads to programmed cell death in target cells, and when combined with IL-1 which acts on the central nervous system causing lethargy (Marieb, 2004). TNFB stimulates granulocyte activity and B cell proliferation which shows an increase in neutrophil count (Jean- Baptise, 2007:63).

The primary function of skin is to form a physical and chemical barrier to the external environment, against injurious insults. Harmful stimuli such as micro-organisms, ultraviolet radiation, toxic agents or irritants evoke a complex response known as inflammation. Inflammation is an essential response in the protection against injurious insults. The five classical signs of acute inflammation are pain, heat, redness, swelling, and functional loss. These signs can be explained by the different phases that the inflammatory response generally follows dilation of capillaries to increase blood flow, vasopermeabilization, leukocyte recruitment elimination of pathogens or injurious stimuli and resolution of inflammation [85]. At the molecular level,

A study involving scientists from Cardiff University set out a range of laboratory experiments involving mice models of asthma and samples of human tissue. With the aim of getting a better understanding of asthma patients and what causes the inflammation of the airways. Results show that as a result proteins called eosinophilic cationic protein (ECP) and other important protein. These proteins carry multiple positive electrical charges. This proved that inflammation is caused by these proteins activating another type of protein molecules called calcium sensing receptors found in the smooth muscle cells that line the airways.

Protease, an enzyme that degrades proteins, then cuts of a small piece of the Protective Antigen. The leftover part of the Protective Antigen then forms into a ring-like structure with six other Protective Antigen-receptor pairs. [4] This creates sites where the Lethal Factor and Edema Factor can attach to the top side of the Protective Antigen. It then deludes the cell, and enters the cell through endocytosis. This creates an endosome with a bubble-like compartment surrounded by a membrane with the toxin-receptor inside. When this moves closer to the Lethal Factor and Edema Factor, it forms a barrel-like pore through the membrane. This is where the toxic Lethal Factor and Edema Factor will be released from to attack targets within the cell.

In the example of TNFa, excessive amounts can be highly cytotoxic and inappropriate expression of this cytokine has been linked to a variety of serious pathological problems such as septic shock (Baer et al., 1998) In view of the potential harm and effects, production of TNFa must be strictly regulated and controlled by negative feedback.

Tachylectin-5A is an ellipsoidal molecule that is an asymmetrical monomer, which is subdivided into three different domains that interact with each other (2). The primary structure of Tachylectin-5A constitutes 269 amino acid residues (1). The amino acid composition of this protein has a cis-peptide bone between Arg-218 and Cys-219 (3). It contains one protein modification called prryolidone carboxylic acid, which is the twenty-fourth amino acid in the sequence (1). And the secondary structure of the protein consists of 16% alpha helical and 24% beta sheets. There are 9 helices with 44 amino acid residues and 19 beta sheets with 66 residues involved in total (1). The

Rheumatoid arthritis treatment is primarily aimed at symptom relief, as there is no cure for this disease. The medicines reduce pain and inflammation in the joints and slow down further progress of the disease. Physical and occupational therapy teaches you to protect the joints. And surgery is done when the joints are damaged severely because of the disease.

Trypsin is a proteolytic enzyme, and is known to be a digestive enzyme found in the small intestine (McDowall, 2018). It has the ability to hydrolyze peptide bonds (The Columbia University Press, 2018). Trypsin enzymes specifically target peptide bonds in molecules that have carboxyl groups donated by the amino acids arginine and lysine (The Columbia University Press,

Allergic conjunctivitis is an inflammatory disease (1) that is initiated by production of pro-inflammatory mediators including histamine, leukotrienes, and prostaglandins that cause edema and recruitment of neutrophils, macrophages, and mast cells (2). The infiltrating leukocytes switch from producing pro-inflammatory mediators to generating the pro-resolution mediators lipoxins, resolvins, protectins, and maresins (2-5). These compounds actively terminate inflammation by blocking the effects of the pro-inflammatory mediators on their target tissues including the conjunctival goblet cells (GC).

Tumour necrosis factor-alpha (TNFa) is a pro-inflammatory monocyte derived cytokine identified as initiating a number of crucial cell mechanisms, largely within the regulation of immune cells and host defence. It is secreted primarily by macrophages and monocytes in response to a bacterial challenge or tumour. Although TNFa is mainly produced by macrophages, it is also produced by a broad variety of other tissues including (but not limited to) endothelial cells, mast cells, fibroblasts and lymphoid cells.