The Difference Between Steroid And Peptides Biology Essay


Peptide hormones act by binding themselves to receptors that they affect thereby inducing a cascading effect. Peptides have charges on them which do not allow them to cross the lipid bilayer on their own. This is the reason they have to attach themselves to the receptors found on then cell membrane where it establishes a cascade by making use of GPCRs and the CAMP. Their main functions include energy storage, foundation for cell membranes and also the foundations for hormones. The fact is that any molecular cell having charges is not able to penetrate the lipid bilayer on it own and therefore needs the aid of receptors which transport them through the layers. Steroids hormones on the other side, act by traveling to the nucleus where they have major effects on the cell. Furthermore, peptides are structurally composed of amino acids which are the building blocks while steroids are described as elements of the plasma membranes and do not contain fatty substances. The steroid hormones are very important in linking a broad variety of very important physiological functions in the body. Steroids regulate body activities during pregnancies; they also regulate anti-inflammatory driving forces within the body.

Pertussis and Cholera toxins

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Pertussis is a toxin a type of protein-based exotoxin that is produced by a bacterium known as Bordetella pertussis, it causes whooping cough. Pertussis colonizes the respiratory track hence causing infections that leads to whooping cough. Pertussis is normally released in an inactive form; it is then embedded to a cell membrane receptor and is taken up in an endosome. After the Pertussis has been taken up in an endosome, it is transported through a process known as retrograde transport to the trans-Golgi network and also through endoplasmic reticulum. In the process of the transport, the activation of protomer takes place, probably through glutathione and ATP. Pertussis toxin acts as catalyst to ADP-ribosylation of the sub-parts of the G-proteins which thwart the interaction between G-proteins and the G-protein coupled receptors that are found on the cell membrane. This finally interferes with the intercellular communications. The consequence of this scenario is that the Gi subunits stay locked within their GDP-bound which is an inactive state and is therefore unable to restrain adenyl cyclase activities. The consequence of this is an increased concentration of cAMP. The rise in intercellular cAMP has adverse effects normal biological signaling. The Pertussis toxins results into several systemic impacts; amongst these impacts are the rise in the release of insulin which in turn leads hypoglycemia.

The cholera toxin has a catalytic potion that only performs just a single task. The portion seeks out the G proteins that are used for cellular signaling and then embeds an ADP molecule to the G-proteins. These actions transform the G-proteins into lastingly active state which implies that it is continuously sending signals. This process causes a lot of confusion to the cells and besides, it commences the transportation of a lot of water and sodium to the outsides. The consequence of this is that it causes flooding in the human intestines thereby resulting into life threatening dehydration or cholera.

The factors that control progression through each of the major phases of the cell cycle

The cell cycle is composed of four distinctive phases which include, G1 phase, S phase, G2 phase and M phase. There G0 referred to as a resting phase; the resting phase implies that the cell is no longer kin the cycle and has stopped the process of dividing. In G1, the size of the cell increases. The checkpoint at G1 control technique is responsible for ensuring that everything necessary is prepared for the synthesis of DNA. At the S phase or synthesis phase the process of the replication of the DNA takes place. G2 represents the gap that is found between the synthesis of DNA and mitosis. The check point at G2 control technique has the responsibility of ensuring that all necessary things are ready to get into the M phase, otherwise known as the mitosis phase and divide. M phase is the stage where cell growth ceases and then the cellular energy is concentrated in the orderly separation of the cell into two daughter cells.

The exogenous pathway of cholesterol metabolism

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In the exogenous pathways, the cholesterols coming from the dietary and from biliary get absorbed into the intestine where it subsequently enters the main circulation as a constituent of chylomicrons. After this, the selective inhibitors of cholesterol absorption give a totally different approach in the hypercholesterolemia management. In this status, the ezetimibe hinders the absorption of biliary and dietary cholesterol in the intestine. After this takes place, the process lowers the total amount of cholesterols along with low density lipoprotein cholesterol levels (LDL-C) in the body of a human being. After hindering the absorption of cholesterol in the intestine, and subsequently lowering the cholesterol content of chyomicrons, the ezitimibe is also likely to reduce the latent atherogenicity of chylomicrons and their residues the amalgamation therapy that takes place between the ezetimibe and statins may be expedient to reduction in low-density lipoprotein cholesterol level.

The process of Fas L (Fas Ligand) induced apoptosis

Fas shape the Death Inducing Signaling Complex upon tendon binding. The Fas ligament trimer found on the surface of the adjacent cell and is anchored on the membrane results into the trimerization of the Fas receptors. Upon resulting aggregation of DD, the receptor complex gets internalized through the cellular endosomal machinery. The adaptor molecule FADD then binds the death domain of Fas via its own the domain. Examples of situations where the system is triggered include during T-cell homeostasis, during cytotoxic T-cell activity.

Atherosclerosis is a multifactorial disease process

Atherosclerosis is a multifactorial disease where by lipoprotein modified by oxidation process plays a major role. Oxidatively modified LDL triggers the disease process by stirring up the articulation of inflammatory genes. Recent theoretical studies have indicated that serum amyloid A contributes to the formation of cholesterol laden foam cells that is detected within the atherosclerotic lesion. During hyperlipidemia, progressive oxidative adjustment of the entrapped lipoprotein within the walls of the artery is vital in inducing all the constituents of the atherosclerosis reaction.

The meaning of cancer

Cancer is also known as malignant neoplasm. It is a category of diseases whereby a group of cells displays the characteristics of uncontrolled growth, invasion and in some cases metastasis. Cancers are brought about by observable abnormalities in the genetic materials found in the transformed cells. The abnormalities causing cancer are normally as a result of tobacco smoking, radiation and other infectious agents.

How the HIV-1 interferes with cellular signaling

HIV-1 is a crucial factor in AIDS pathogenesis. HIV-1 potently hinders motility of fibrobrist and the chemotaxis of HIV-1 contaminated primary T lymphocytes of human beings toward the chemokines, CCL-19 and also CCL-21 ex vivo. Moreover, Nef hinders guided motility of the Zebrafish primordial germ cells on the way to endogenous ADF-1a in vivo. The resulting migration defects are a consequence of Nef-aided inhibition caused on actin remodeling which is usually activated by the migratory stimuli. Nef stimulates phosphorylation of cofilin thereby inactivating the evolutionarily preserved actin-depolymerizing factor that is responsible for the promotion of cell motility when it is unphosphorylated.