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Mapping protein signal pathway interaction in sarcoma …

not signal peptide triggered protein secretion

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Using the signal peptides, the hyper-protein secretion system was ..

The method incorporates a prediction of cleavage sites and a signal peptide/non-signal peptide prediction based on a combination of two artificial neural networks.

07/05/2013 · The signal peptide plays a key role in targeting and ..

Perfused TissueTissues are continuously perfused by serum -- their histopathology may be reflected in serum proteomic “patterns.”Patterns of Proteomic Information in SerumHypothesis: 1. Signature proteins are products of the tumor-host microenvironment, and thereby unique to the tissue site and pathophysiological state.2. These biomarkers are likely to be modified or cleaved “reporter” proteins/peptides that are produced/amplified at the tumor/host interface, are released, and partition to circulating carrier proteins.

JCI - FGF21 is an endocrine signal of protein restriction

18/08/2014 · FGF21 therefore represents an endocrine signal of protein ..

The signal hypothesis, a widely disseminated explanation for how proteins are transported across the membranes of living cells, may be heading for partial derailment.

Two research groups, one based at the Institut Pasteur in Paris and the other at Massachusetts Institute of Technology in Cambridge, have just published carefully worded challenges to the signal hypothesis as it pertains to bacteria [ , 286 , 356 (1980), and , 20 , 749 (1980)]. The challengers suggest that the simple terms of the signal hypothesis aren't "sufficient" to explain new genetic and biochemical information. In offering these criticisms, the scientists don't recommend scrapping the hypothesis altogether, although other critics have done so during the past several years.

Translocation of proteins across membranes: the signal …

Post‐translational processing and trafficking of secreted and transmembrane proteins in neurons: (a) During and after translation, secreted and transmembrane proteins receive post‐translational modifications (text, left) as they pass through the endoplasmic reticulum (ER), Golgi apparatus and ‐Golgi network (TGN). Finally, vesicles containing the proteins bud from the TGN and are transported to their final destination. Targeting mechanisms guide the vesicles to the axon or dendrites and then to the correct area within each where they are secreted or inserted into the plasma membrane. In a process called transcytosis (centre), some axonal membrane proteins are first inserted into the dendritic plasma membrane and then reinternalised and trafficked to the axon. (b) Transmembrane proteins, including neurotransmitter receptors, can also be removed from and inserted into the membrane at synapses. Stimulation changes the number of receptors at a synapse which determines the magnitude of synaptic transmissions. On the presynaptic side there are clear vesicles that contain conventional neurotransmitters (e.g. glutamate, GABA) as well as dense‐core vesicles that contain neuropeptides. (c) Many neuropeptides are produced by cleavage of a single large precursor called a prepropeptide in the Golgi and the TGN. Illustrated, a precursor called proopiomelanocortin (POMC) is cleaved up to 8 times to form up to 10 different neuropeptides. (From Castro and Morrison .). (d) As a transmembrane protein is translated, signal sequences in the protein cause it to cross the ER membrane in a certain orientation. Secreted proteins cross the ER membrane a single time. Multiple signal sequences can cause the protein to cross the ER membrane many times (not shown). Adapted from Lodish .

The method incorporates a prediction of cleavage sites and a signal peptide/non-signal peptide prediction based on a combination of several artificial neural networks.

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    Molecular Diagnostics New Target Discovery (Global Proteomics) Signal Transduction Pathway ..

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Low Protein Intake Is Associated with a ..

Biochemical networks called signal transduction pathways convert specific patterns of synaptic transmissions into new protein synthesis. Ribosomal and RNA‐binding proteins are common targets of these pathways.

Sturge–Weber Syndrome and Port-Wine Stains Caused …

Signal transduction pathways that lead to translation and transcription in neurons. Extracellular ligands bind cell surface receptors coupled to cascades of molecular interactions that cause translation and transcription. Note that most pathways directly or indirectly target the initiation complex, formation of which is the rate‐limiting step in translation. The pathways illustrated are greatly simplified. A single type of receptor can activate many pathways and different pathways interact extensively. Each pathway ‘component’ is often a complex of subunits. After a pathway is activated, additional molecules are required to deactivate it as well as the transcription and translation that it triggers (not shown).

Signal Hypothesis | SpringerLink

Neurons are immensely complex cells whose morphology and physiology underpin our cognition. Achieving proper neuronal connections during development, as well as eliciting appropriate responses to environmental stimuli in the adult, requires precisely regulated protein synthesis. To meet these requirements, neurons have adapted regulatory mechanisms that act at every step in the process of producing functional proteins. Many of these mechanisms target messenger ribonucleic acid (mRNA)‐binding proteins and ribosomal subunits to regulate translational initiation. These mechanisms are especially concentrated at synapses, where they act to transform transient electrical signals into lasting functional modifications that are a basis for learning and memory. Misregulated synaptic protein synthesis contributes to several human cognitive changes including addiction, fragile X syndrome and autism.

According to the signal hypothesis ..

We applied reverse phase protein microarrays technology to map signal pathway interactions in a discovery set of 34 soft tissue sarcoma (STS) bone metastases compared to healthy bone. Proteins associated with matrix remodeling (MMP), adhesion (FAK Y576/577, Syndecan-1), and growth/survival (IGF1R Y1135/1136, PI3K, EGFR) were elevated in metastasis compared to normal bone. Linkage between Syndecan-1, FAK Y576/577, Shc Y317, and EGFR, IGF Y1135/1136, PI3K/AKT was a prominent feature of STS bone metastasis. Elevated linkage between RANKL and 4EBP1 T37/46, EGFR, IGF1R Y1135/1136, Src Y41, Shc Y317, PI3Kp110γ was associated with short survival. Finally, we tested the hypothesis that signal pathway proteins augmented in the STS bone metastasis may provide clues to understand the subset of primary STS that metastasize. The most representative molecules identified in the discovery set were validated on an independent series of 82 primary STS by immunohistochemistry applied to a tissue microarray. The goal was to correlate the molecular profile in the primary tumors with a higher likelihood of metastasis. Elevation of activated kinase substrate endpoints IRS1 S612, 4EBP1 T37/46, FAK Y576/577 and loss of Fibronectin, were associated with a higher likelihood of metastases. These data indicate that the linkage between matrix remodeling, adhesion, and growth signaling may drive STS metastasis and can be the basis for prognostic and therapeutic strategies.

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