Tyrosine kinase Essays

From the 1990’s movie entitled Awakenings directed by Penny Marshall. A sprung of hope has happened to people who suffered the post-effect of the 1920’s epidemic disease called Encephalitis Lethargica by bringing them back to their mobile bodies for a limited time by the neurologist, Dr. Malcolm Sayer. Encephalitis Lethargica, also known as sleeping sickness, is viral epidemic encephalitis that occurred between 1915 and 1926 and those who survived the initial infection displayed long-term apathy

Mechanisms of DOM There are many theories that have been researched in order to explain why an individual experiences DOMS. Theories include but are not limited to: enzyme efflux, lactate formation, muscle spasm, connective tissue damage, muscle damage and inflammation (Cleak, Gulick). Researchers suggest that not one single theory can be directly correlated to the effects of DOMS. The unique sequence of events from all possible modules contributes to the effects that an individual might experience

threonine, tryptophan, and valine. Phenylalanine, one of the essential amino acids, is used in the body to form tyrosine. An enzyme called phenylalanine hydroxylase is involved in adding a hydroxyl group to phenylalanine in what is called a hydroxylation reaction to form tyrosine (Pratt 485). Since tyrosine can be produced in humans in this way, it is considered a nonessential amino acid. Tyrosine is also found in foods such as avocados, pumpkin seeds, bananas, and various dairy products (University of

activates MAP2K, which activates MAPK. MAPK can now activate a transcription factor, such as MYC. In more details, receptor-linked tyrosine kinase as the epidermal growth factor (EGFR) is activated by extracellular ligand, epidermal growth factor (EGF). This activates the tyrosine kinase activity of the cytoplasmic domain of the receptor. The EGFR becomes phosphorylated on tyrosine residues. Next, GRB2 binds to the phosphotyrosine residues of the activated receptor. Then GRB2 binds to the guanine exchange

Explain how targeted therapy works ( in the treatment of cancer), and evaluate its effectiveness in treating cancer. You may wish to focus on a specific type of cancer Name - Vipanpreet kaur Student ID - 39298 Class - HAS-3 Word count- 1223 Targeted therapy

- the M-BCR region located on chromosome 22 - which causes the formation of a BCR-ABL fusion gene. This fusion gene, according to Shet, Jahagirdar and Verfaillie (2002), will produce an onco-protein (p210BCR/ABL) that not just results in more tyrosine kinase (TK) activity, rather than also in increased binding to the actin cytoskeleton; an unregulated growth factor; an accelerated proliferation of leukemic hematopoietic cells; as well as an increased resistance of progenitors/precursors to apoptosis

hybridization). BCR -ABL contains a protein that plays an important role in development of leukemia & it is BCR-ABL oncogene. Imatinib & Nilotinib are used for its treatment. Imatinib mesylate (Glivec, Novartis), a potent competitive inhibitor of the tyrosine kinase

Abstract Angiogenesis is a physiological process that causes the growth of new blood vessels from pre-existing vessels. This process is regulated both by activating molecules and inhibitors of angiogenesis and also played a key role in physiological processes such as organ growth and development, wound healing and reproduction and in the pathological process of tissue destruction including tumor growth, metastasis, arthritis, etc. Generally, process of angiogenesis is influenced by several factors

and 3 also have a kinase inhibitory domain (KIR) located adjacent to the SH2 domain which is used to inhibit JAKs62,66. SOCS regulate JAK/STAT pathway in three ways. The first method is that SOCS associate with phosphorylated tyrosine residues on JAKs to prevent JAKs phosphorylating the cytokine receptor which allows STATs to bind so JAKs can phosphorylate and activated them. SOCS bind to the JAKs via their KIR domain1,58. The Secondly SOCS associate with the phosphorylated tyrosine residues on the

achondroplasia (ACH) Achondroplasia (ACH) is a very rare (fewer than 20,000 US cases per year) yet the most common (occurring at one in every 15,000 to one in 40,000 live births) hereditary form of short-limbed dwarfism. Achondroplasia can be inherited from a parent with the disease, however most cases of ACH are because of new mutations in the FGFR3 gene. (Over 80% of people with ACH have parents who are unaffected). People with achondroplasia have a short stature and normal sized torso. An adult

Medicine has come a long way from taking roots and plants and making vaccines and medication. Although most medicine is beneficial, some do not help or fight diseases in certain people’s bodies. Precision Medicine is a modern phenomenon that has recently become a big deal amongst many doctors. Patients who have tried chemotherapy, for example, to disrupt the spread of cancer realize this treatment will not work, and they need a doctor to create personalized medicine to try to cure their disease a

Describe the processes of mitosis and meiosis in details and their functions 
 Introduction Cell division does not stop with the formation of the mature organism but continues in certain tissues throughout life. It is because cell cannot grow any larger. Besides, cell division is necessary for the repair and replacement of aged or dead cells. Moreover, it is necessary for the growth and reproduction. There are two distinct types of eukaryotic cell division: Mitosis and Meiosis. Mitosis leads to

middle. Chromosome abnormalities are also important as t(4;11), trisomy 8, or deletion 7 are poor prognostic indicators. The Philadelphia chromosome used to be thought of as a poor prognostic indicator but now there are targeted drugs (e.g., tyrosine kinase inhibitors) that can improve the overall prognosis. The response to initial chemotherapy also impacts prognosis as those who go into CR (e.g., less than 5% blasts in the marrow and normal blood counts) within 4-5 weeks have better prognosis while

to lipid peroxidation and oxidative DNA loss but can interfere with physiology and intracellular signal transduction. The resulting change in intracellular redox status leads to the activation of protein kinase, for example, tyrosine kinase, protein kinase c, and the mario-activated protein kinase cascade leading to modified cellular functions. Oxidative stress compounds hypothyroidism. Hypothyroidism is a state that increases the oxidative stress. In this study, the biomarker is high in MDA level

of drugs that specifically “attack malignant cells while leaving normal cells unharmed” is being researched. An example of targeted therapy is designing a drug that can disrupt “molecular signaling pathways, such as those that use the protein tyrosine kinases” (Porth,

Insulin, a polypeptide hormone, is one of the most important pancreatic islets, more specifically the islets of Langerhans(named after the scientist who discover them) produced by the beta cells. These cells( beta cells) are mainly responsible for extracting glucose from each carbohydrates and help the body to either use it or store it for later use. Insulin plays a vital role in regulating blood glucose level by preventing it from getting too high(hyperglycemia). Glucose is the main source of energy

designated as PKU is defined as an inborn error of metabolism due to deficiency of the enzyme phenylalanine hydroxylase (PAH). This is a rare genetic condition in which occurs inability to metabolise or break down the essential amino acid phenylalanine to tyrosine due to enzyme deficiency. Amino acids are considered as the building blocks of protein and so does this amino acid i.e. phenylalanine. Phenylalanine is an essential amino acid and hence, finds a role in protein synthesis in our body. Certain sources

cancer chemotherapy which includes toxicity, side effects and lack of tumor selectivity. TDDS for cancer takes advantage of the growing number of tumor specific cell surface molecular biomarkers to design targeted delivery modules. EphA2 receptor tyrosine kinase is one of the therapeutic target for cancer. Antibody-drug conjugate (ADC) and peptide-drug conjugate (PDC) has been exploited to deliver cytotoxic drug to EphA2 expressing cells. This paper therefore describes both conjugates, its pros and cons

phase, and blastic crisis. The first phase is the chronic phase. Patients in this phase have less than 10% of immature white blood cells. The symptoms are mild with frequent infections, tiredness, and indigestion. The main treatment is a tyrosine kinase inhibitor (TKI) such as imatinib, nitotinib, or dasatinib.

Binding causes auto-phosphorylation of tyrosine residues in the receptor protein, and the receptor interacts with insulin receptor substrate molecules in the cell. These are phosphorylated, interact with phosphatidylinositols, and this carries on the signalling cascade via PI3 kinase which activates translocation of vesicles containing pre-formed GLUT4 proteins from within the cell to the cell membrane, where