Receptor tyrosine kinase

1.1 Diabetes mellitus and Insulin resistance Diabetes mellitus, or simply diabetes, is a metabolic disorder that is marked by hyperglycemia, high blood glucose. In 2014, 29.1 million individuals in the United States, which is about 9.3% of the population, have diabetes . Among all cases of diabetes, about 90% to 95% are Type 2 Diabetes (T2D), the diabetes form generally results from defects in insulin action . Furthermore, other related complications of diabetes will afflict patients with their cardinal

membrane and tubulin-tyrosine ligase activity, respectively. Mitochondria is the basic and important organelle in most of the eukaryocyte. Mitochondria outer membrane permeabilization has been reported to be involved in cancer and be a promising therapeutic target. [26-27] Thereby, miR-193a-5p might be also involved in lung cancer through similar approach. Recently, Tubulin tyrosine ligase widespread loss has been found during the tumor growth, which suggests tubulin tyrosine ligase activity may be

itself1. It has recently been shown that overactivity of glycogen synthase kinase 3 (GSK-3) may be implicated in the impaired insulin action2. Although GSK-3 is a distal element of the insulin signaling pathway (which includes insulin receptor substrate 1 or IRS-1), when it is overactive, this affects both insulin signaling and the removal of glucose from the blood stream by skeletal muscle. Firstly, when

growth factor receptors (HER1 to HER4) are a family of receptors, those expressed in many types of cancer and normal tissues. The HER2 is the dominant TK receptor in breast cancer, approximately 20% of all breast cancers. It is activated by homo- or heterodimerization with other family members, and phosphorylated HER dimmers activate downstream regulation of MAPK pathway, PI3K, and signal transducer and activator of transcription pathways (Serra et al., 2011). Mitogen-activated protein kinase (MAPK) or

The first oncogene targeted anti-cancerous agents are Gleevec and Herceptin. Gleevec is a small molecule designed to target tyrosine kinase (enzymes that activate many proteins by signal transduction cascades) encoded by bcr/abl oncogene. Herceptin is a monoclonal antibody which interferes with the receptors responsible for activation of proteins which signal cell proliferation. It was earlier thought that up to seven independent genetic hits are necessary for the

decreases blood glucose levels, while glucagon increases them.(2b) The way insulin works is it targets any cell, except, red blood cells, and activates the receptor Tyrosine Kinase and recruits substrate adaptors, IRS family proteins. Tyrosine phosphorylated IRS then displays binding sights for numerous signaling partners. This binding alters the receptor protein. All of this can result in the increase of the cellular uptake of glucose. While the process of insulin is difficult, glucagon is much simpler

LRRK2 Kinase activity of mutant LRRK2 has been shown to mediate neuronal toxicity and cell death in PD (Smith et al., 2006). The BRAF kinase which is believed to cause a significant proportion of melanoma is similar to the kinase domain of LRRK2, which is known to drive a significant proportion of malignant melanoma (Bishop et al., 2009; Flaherty et al., 2010; Flemming et al., 2010; Paisan Ruiz et al., 2010; Shen J et al., 2004), implying that there could be functional analogies between the activation

recognise and bind to specific receptors on the target cell. In order for the signal to be generated in most cases there has to be an environmental change. Cells detect signals with Cell Receptors on their plasma membrane. The signalling molecule binds to the Receptor because its shape and chemical complexity. This then activates a chain of reactions within the cell, leading to a range of different responses. Cells have a mechanism that allows

cancers that RAS oncogenes can cause the frequency of mutations in certain cancers and the different isoforms of RAS. A major breakthrough from 1987 - 1993 started to shed light on the signalling mechanisms of RAS; how RAS is activated by receptor tyrosine kinases, how RAS associates with GEF’S (guanine exchange nucleotide factors) and GAP’S (GTP-ase activating proteins); how RAS is associated with downstream signalling pathways involved in key cellular processes, and how tumour cells harbour oncogenic

One of the most common treatments for heart failure is ACE inhibitors. ACE inhibitors have shown to slow down the course of heart failure and decrease cardiovascular mortality (1). Overall, they work by suppressing the activity of angiotensin II. ACE inhibitors prevent the conversion of angiotensin I to angiotensin II by competitively inhibiting the activity of the angiotensin converting enzyme. Since angiotensin II is a vasoconstrictor, the lack of the protein allows blood vessels to remain dilated