Extracellular signal-regulated kinases

Introduction Axonal death is a main element in many neurodegenerative diseases. It has been observed in many neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Axon degeneration does not necessarily have to involve the typical apoptotic pathway regardless of the morphological similarities to cells undergoing apoptosis. Yang et al. focused on axonal death in traumatic injury because it has been shown to be independent of the necroptotic pathway. This was discovered since

Earth to exist. There are several types of cellular signalling (neural, endocrine, exocrine, paracrine, autocrine). In most cases signals are released by signalling cells. These signalling molecules 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

receptor TKs, transducer signals from extracellular to the cytoplasm but the non RTKs are intracellular, it transmits intracellular signals (Pawson, 2002). For example the known RTKs of EGFR and platelet derived growth factor receptors (PDGFR) are monomers placed in the cell membrane. When the ligands were binding to their extracellular domain resulting RTKs are activated. The ligands of epidermal growth factor (EGF), platelet derived growth factor (PDGF) etc., are extracellular signal molecules that induce

specific signals or ligands that fit into it. JAK stands for Janus kinase, Janus is the Greek word for god of transition and kinase is any type of enzymes that phosphorylate, giving energy by adding phosphate group, any type of proteins. JAK contains JAK tyrosine kinases which are the enzymes that can convey a phosphate group from adenosine triphosphate (ATP) to another protein. There are four different types of JAK proteins: Tyk2 (Tyrosine kinase 2), JAK 1, JAK2, and JAK3. STAT stands for signal transducers

and collaborators identified novel MECP2-regulated miRNAs during the human prenatal neurodevelopment. Utilizing human patient- and MeCP2 knockdown-derived monolayer neuronal culture and organoids models, they found an upregulation of the expression levels of miR-199 and miR-214 and their downstream targets (PAK4 and PTEN, respectively), that differentially regulate extracellular signal regulated kinase (ERK) and mitogen-activated kinase and protein kinase B (PKB/AKT) signalling pathways upstream

Introduction: Cell behavior is regulated by numerous environmental signals with associated alterations in the expression of various genes involved in cellular physiology. As result, protein synthesis is consequently downregulated, therefore having a negative impact on growth and proliferation. An understanding of the mechanisms by which cells receive and integrate extracellular signals, triggering a cascade of intracellular signals that influence cell growth and metabolism, is essential to developing

gene. When the mutated fibroblast growth factor receptor 3 protein interacts with a fibroblast growth factor ligand, the receptor is stabilized and a cascade of events occur. Downstream receptor pathways that are affected by the mutation involve signal transducer and activator of transcription 1 and phospholipase C, gamma 1. Different mutations on the fibroblast growth factor receptor transmembrane

meant, by the term “receptor desensitization.” What does it mean when we say that the receptor is “uncoupled” versus “down-regulation” of the receptor? Define and contrast the roles of the “second messenger-dependent” protein kinases versus the “G protein-coupled receptor” kinases in the process of receptor desensitization. What do the terms “homologous” versus “heterologous” desensitization refer to? (Ferguson, Pharmacological Reviews 53:1-24, 2001; Gainetdinov et al., Annual Review of Neuroscience

target genes which ultimately play a crucial role in cellular viability, survival, apoptosis, etc. (1,2) Activation of the JAK/STAT pathway is responsible for initiation of multiple signal transduction cascades such as Ras-Raf-MEK-Erk, PI3K-Akt-mTOR and phospholipase C-γ. Excessive stimulation of cytokine regulated cascades is seldom unaccompanied by adverse events. Negative regulation as such is accomplished by protein tyrosine phosphatases (e.g. SHP-1, CD45) which act by removing phosphates from

localizations 18,51,54. The EAVK sequence, as part of the first intracellular loop in CaCCs, is regulated by alternative splicing 51 and believed to have a pivotal role in biophysical and gating properties of the channel 43. Besides alternative splicing as a posttranscriptional modification that modulates the activity