Pub med result3
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1) The document discusses neuropeptide G-protein-coupled receptors, their cognate ligands, and behavior in the nematode Caenorhabditis elegans. 2) The identification of peptide ligands for a G-protein-coupled receptor in C. elegans has provided insight into the neuronal circuitry regulating feeding behavior. 3) Studies in C. elegans have identified several putative peptide G-protein-coupled receptors implicated in reproduction and locomotion, suggesting these receptors are targets for discovering novel anthelmintic agents.
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![PubMed Results<br />Item 1 of 1<br />1.Trends Pharmacol Sci. 2005 Feb;26(2):56-8.Neuropeptide G-protein-coupled receptors, their cognate ligands and behavior in Caenorhabditis elegans.Geary TG, HYPERLINK quot;
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kubiak%20TM%22%5BAuthor%5Dquot;
quot;
_blankquot;
Kubiak TM.SourcePfizer Animal Health, Veterinary Medicine Pharmaceuticals Discovery Research, 7000 Portage Road, Kalamazoo, MI 49001, USA.timothy.g.geary@pfizer.comAbstractDespite a simple nervous system, the free-living nematode Caenorhabditis elegans exhibits complex behaviors. The identification of peptide ligands for a G-protein-coupled receptor (GPCR) has provided insight into the neuronal circuitry involved in the regulation of feeding behavior in this worm. Progress in this regard has been accelerated by the discovery that functional expression of worm GPCRs in mammalian cells can be highly temperature dependent. Gene silencing and behavioral analysis has further identified several putative peptide GPCRs that are implicated in reproduction and locomotion. These studies suggest that these peptide GPCRs are legitimate targets for the discovery of novel anthelmintic agents.PMID:15681019[PubMed - indexed for MEDLINE]<br />](https://image.slidesharecdn.com/pubmedresult3-110523214933-phpapp02/85/Pub-med-result3-1-320.jpg)
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GENETIC VARIATION IN G COUPLED PROTIEN RECEPTORS
1. Genetic variations in G protein-coupled receptors (GPCRs) can contribute to differences in disease susceptibility and drug responses, as GPCRs are commonly targeted by pharmaceutical drugs.
2. GPCRs represent the largest family of membrane receptors and are involved in many physiological processes. Variations in GPCR DNA sequences can alter the structure and function of GPCRs and their coupling to other proteins.
3. Single nucleotide polymorphisms account for the majority of genetic variations and can affect domains of the GPCR involved in ligand binding, G protein coupling, and intracellular signaling pathways. These variations may lead to constitutive receptor activation or enhanced signaling associated with genetic disorders.
G protein coupled receptor(gpcr)
This document discusses G-protein coupled receptors (GPCRs):
- GPCRs are the largest family of transmembrane receptors and play important roles in human senses and physiology. They respond to a wide range of ligands.
- GPCRs are classified into families based on sequence homology and functional similarity. The largest family is rhodopsin-like receptors which have 7 transmembrane domains.
- GPCRs are activated via conformational changes in the transmembrane domains, primarily involving movements of "microswitches" that allow the receptor to activate associated G proteins and downstream signaling.
Genetic variations in gpcr
Genetic variations in G protein-coupled receptors (GPCRs) can alter receptor function and cause diseases. Single nucleotide polymorphisms and other mutations have been linked to impaired or enhanced receptor signaling. For example, a mutation in the vasopressin V2 receptor causes nephrogenic diabetes insipidus by decreasing ligand binding and receptor expression. Similarly, mutations in chemokine receptors CCR5 and CCR2 impact HIV infection by altering receptor function or interaction with other coreceptors. Overall, GPCR polymorphisms are associated with diseases by changing ligand binding, receptor activation, trafficking, and coupling to downstream signaling pathways.
Receptor Effector coupling by G-Proteins Zarlish attique 187104
This document is a PowerPoint presentation by Zarlish Attique on the topic of receptor-effector coupling by G-proteins. It discusses how G-proteins transmit signals from stimuli outside a cell to its interior through conformational changes when ligands bind to G-protein coupled receptors. This causes the G-protein's alpha subunit to exchange GDP for GTP, dissociate from other subunits and bind to effector proteins like enzymes to transmit signals via second messengers. Common types of G-proteins include Gs, Gi, Go and Gq. The presentation provides details on the structure and function of G-protein coupled receptors and G-proteins, and gives adenyl cyclase as an example of the
Genetics variations in gpcr
G-proteins are molecular switches that regulate various cellular activities. They exist in two classes: monomeric small GTPases and heterotrimeric complexes consisting of α, β, and γ subunits. G-protein coupled receptors (GPCRs) have seven transmembrane domains and interact with G-proteins via intracellular loops to transmit extracellular signals within the cell. Genetic variations in GPCRs can affect receptor functions like ligand binding and G-protein coupling, potentially causing diseases. Many single nucleotide polymorphisms and mutations have been linked to impaired or enhanced receptor signaling and diseases ranging from bleeding disorders to asthma, obesity, and immune deficiencies.
GH and IGF Research 2014 OR3-4
- The study examined the effects of overexpressing growth hormone (GH) in the basolateral amygdala of rats. It found that GH overexpression dramatically increased the density of dendritic spines on neurons in this brain region, suggesting that GH promotes dendritic spinogenesis and neuronal growth. This reveals a novel role for GH in the adult brain.
- The increased dendritic spine density provides a potential mechanism for how chronic stress, which enhances GH levels in the amygdala, could alter amygdala structure and function and contribute to stress-induced changes in fear memory.
Cell signalling 2
This document discusses G protein-coupled receptors (GPCRs), which are the largest family of membrane receptors in the human genome. GPCRs have seven transmembrane domains and signal by interacting with G proteins. They regulate many important physiological processes and are involved in many diseases. The document outlines the structure and function of GPCRs and G proteins, including how GPCRs activate G proteins, the different classes of GPCRs, mechanisms of GPCR regulation like phosphorylation and desensitization, and the roles of GTPases in general.
emm201548a
N-acetyl-D-glucosamine kinase (NAGK) interacts with dynein light-chain roadblock type 1 (DYNLRB1) at dendritic branch points in neurons. Immunocytochemistry and proximity ligation assays showed colocalization of NAGK and DYNLRB1 on microtubule fibers at dendritic branches. NAGK was also found to interact with Golgi outposts and DYNLRB1 at branch points, indicating a tripartite interaction between NAGK, dynein, and Golgi that regulates dendritic growth and branching. Introduction of a peptide derived from DYNLRB1 stunted dendrite development in cultured neurons.
Genetic variation in G protein coupled receptors
This document discusses genetic variation in G protein-coupled receptors (GPCRs). It notes that GPCRs are membrane proteins involved in cell signaling and the targets of many drugs. Genetic variations can influence drug efficacy and safety through several mechanisms: by altering the structure and function of GPCRs, their coupling to G proteins and signaling pathways, their binding pockets, and their spontaneous signaling. Specific examples of genetic variations in GPCRs that are associated with human diseases are also provided.
genetic variation in gpcr and its disease due to variation
1. GPCRs are the largest family of membrane receptors and are important drug targets. They signal through heterotrimeric G proteins and can exist in multiple conformations to trigger distinct pathways.
2. Genetic variations in GPCRs, such as single nucleotide polymorphisms, contribute to inter-individual differences in disease susceptibility and drug responses. Variations can impact receptor structure and function, G protein coupling, and ligand binding pockets.
3. Some GPCR variations are associated with diseases. For example, mutations in vasopressin V2 receptors cause nephrogenic diabetes insipidus by producing non-functional receptors, while mutations in chemokine receptors protect against HIV infection.
Disrupted development and altered hormone signaling in male Padi2:Padi4 doubl...
Background: Peptidylarginine deiminase enzymes (PADs) convert arginine residues to citrulline in a process called citrullination or deimination. Recently, two PADs, PAD2 and PAD4, have been linked to hormone signaling in vitro and the goal of this study was to test for links between PAD2/PAD4 and hormone signaling in vivo.
Methods: Preliminary analysis of Padi2 and Padi4 single knockout (SKO) mice did not find any overt reproductive defects and we predicted that this was likely due to genetic compensation. To test this hypothesis, we created a Padi2/Padi4 double knockout (DKO) mouse model and tested these mice for a range of reproductive defects. Results: Controlled breeding trials found that DKO breeding pairs, particularly males, appeared to take longer to have their first litter than wild-type FVB controls (WT), and that pups and DKO male weanlings weighed significantly less than their WT counterparts. Additionally, DKO males took significantly longer than WT males to reach puberty and had lower serum testosterone levels. Furthermore, DKO males had smaller testes than WT males with increased rates of germ cell apoptosis.
Conclusions: The Padi2/Padi4 DKO mouse model provides a new tool for investigating PAD function and outcomes from our studies provide the first in vivo evidence linking PADs with hormone signaling.
Gpcr genetic variation
Genetic variations in G protein-coupled receptors (GPCRs) can lead to changes in receptor structure and function resulting in disease. GPCRs interact with G proteins and undergo conformational changes upon ligand binding to signal inside cells. Single nucleotide polymorphisms account for most genetic variations and can occur in transmembrane domains, extracellular/intracellular loops, or terminal tails. Variations may affect ligand binding pockets, G protein coupling, or cause constitutive receptor activation. This can result in impaired or enhanced receptor signaling causing diseases like nephrogenic diabetes insipidus or bleeding disorders. Several examples of variants in receptors for hormones, chemokines, biogenic amines are described that link genetic changes to associated pathological phenotypes.
G- Protein Coupled Receptors
GPCRs are the most dynamic and most abundant all the receptors. The G protein-coupled receptor (GPCR) superfamily comprises the largest and most diverse group of proteins in mammals. GPCRs are responsible for every aspect of human biology from vision, taste, sense of smell, sympathetic and parasympathetic nervous functions, metabolism, and immune regulation to reproduction. GPCRs interact with a number of ligands ranging from photons, ions, amino acids, odorants, pheromones, eicosanoids, neurotransmitters, peptides, proteins, and hormones.
Nevertheless, for the majority of GPCRs, the identity of their natural ligands is still unknown, hence remain orphan receptors.
The simple dogma that underpins much of our current understanding of GPCRs, namely,
one GPCR gene− one GPCR protein− one functional GPCR− one G protein −one response
is showing distinct signs of wear.
Genetic VaRITION IN GPCR.pptx
G-proteins are proteins that act as molecular switches inside cells and are involved in signal transduction. They have two classes: monomeric small GTPases and heterotrimeric G-protein complexes composed of alpha, beta, and gamma subunits. G-protein coupled receptors (GPCRs) have 7 transmembrane domains and interact with G-proteins via intracellular loops to regulate their activity. Genetic variations in GPCRs and associated proteins can lead to diseases by altering receptor function, such as impaired or enhanced signaling. Single nucleotide polymorphisms in receptors like beta-adrenergic and chemokine receptors have been linked to conditions like asthma and HIV resistance.
GM Food Allergy Biomarkers
The document describes a research study aimed at developing biomarkers for detecting potential allergenicity of novel foods, including genetically modified foods. The researcher conducted experiments challenging mice with known food allergens (egg ovomucoid protein and peanut protein) and analyzed gene expression profiles in the mice spleens. Several hundred genes were found to be differentially expressed. After validating some genes, the researcher identified potential biomarker genes that could help detect allergenicity of GM foods. The study provides insights into transcriptomic responses to food allergens and biomarkers that may help evaluate allergenicity of novel foods like GM crops.
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Receptor Effector coupling by G-Proteins Zarlish attique 187104
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genetic variation in gpcr and its disease due to variation
genetic variation in gpcr and its disease due to variation
Disrupted development and altered hormone signaling in male Padi2:Padi4 doubl...
Disrupted development and altered hormone signaling in male Padi2:Padi4 doubl...
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