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Decapping is a key step in general and regulated mRNA decay. The protein encoded by this gene is a decapping enzyme. This protein and another decapping enzyme form a decapping complex, which interacts with the nonsense-mediated decay factor hUpf1 and may be recruited to mRNAs containing premature termination codons. This protein also participates in the TGF-beta signaling pathway.
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TRPC3 Antibody: The mammalian transient receptor potential (TRP) superfamily can be divided into three major families including the "canonical TRP" (TRPC) family. The seven members of this family share the activation through PLC-coupled receptors and have been suggested to be components of receptor-regulated cation channels in different cell types. Furthermore, the members of the TRPC3/6/7 subfamily can be activated by diacylglycerol analogs, suggesting a possible mechanism of activation of these channels by PLC-coupled receptors. TRPC3 encodes a Ca2+-permeant channel that is agonist-activated but not store-operated or directly receptor-activated. TRPC3 physically interacts with TRPC6 and TRPC7 and forms functional tetrameric channels.
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TANK Antibody: TANK was initially identified as a novel TRAF-interacting protein that regulated TRAF-mediated signal transduction. Specifically, ligand binding by surface receptors in the tumor necrosis factor (TNF) receptor and Toll/interleukin-1 (IL-1) receptor families lead to the formation of a TRAF/TANK complex that mediates the activation of the transcription factor NF-kappa B. This activation of NF-kappa B occurs through an association with the kinases IKK epsilon and TBK1. More recently, it was shown that these proteins can then form a complex with NEMO, a protein that regulates the activity of the I kappa B complex. This suggests that in addition to the possibility that TBK1 and IKK epsilon activate the IKKs, the association with the IKK complex may help these kinases modulate other functions, such as the transactivation potential of NF-kappa B proteins. At least two isoforms of TANK are known to exist.
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STAT3 Antibody: STATs (signal transducers and activators of transcription) are a family of cytoplasmic latent transcription factors that are activated to regulate gene expression in response to a large number of extracellular signaling polypeptides including cytokines, interferons, and growth factors. After phosphorylation by JAK tyrosine kinases, STATs enter the nucleus to regulate transcription of many different genes. Among the seven STATs (STAT1, STAT2, STAT3, STAT4, STAT5a, STAT5b, and STAT6), STAT1, STAT3, STAT5a, and STAT5b have a wide activation profile. STAT3 signals are pivotal to the proliferation and differentiation of neural stem cells and also participate in neuronal regeneration and cancers of the nervous system.
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NELF Antibody: NELF (nasal embryonic luteinizing hormone-releasing hormone factor) is a 530 amino acid transcription factor involved in the migration of LHRH neurons, outgrowth of olfactory axons and suppression of transcription elongation. NELF is found in the peripheral and central nervous system during embryonic development, and is highly expressed in adult testis, kidney and brain. Known to couple NMDA receptor signaling to the nucleus, NELF knockdown impaired GnRH neuronal migration of NLT cells in vitro and the gene encoding NELF has been linked to the development of Idiopathic hypogonadotropic hypogonadism (IHH), a disorder resulting in impaired pubertal maturation and reproductive function.
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PTGDR2 Antibody: The prostaglandin D2 receptor 2 (PTGDR2), also known as CRTH2, is expressed on Th2 cells and eosinophils and mediates chemotaxis of these cells to PGD2 and is thus thought to be a key receptor mediating eosinophil and Th2 recruitment during allergic responses. However, PTGDR2-null mice showed enhanced eosinophil recruitment into the lung consistent with observations that the PTGDR2-null mice produced significantly higher amounts of interleukin-5 (IL-5) and IL-3. This suggests that PTGDR2 plays a nonredundant role in restricting eosinophilia and allergic response in vivo.
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HADH functions in the mitochondrial matrix to catalyze the oxidation of straight-chain 3-hydroxyacyl-CoAs as part of the beta-oxidation pathway. Its enzymatic activity is highest with medium-chain-length fatty acids. Mutations in this gene cause one form of familial hyperinsulinemic hypoglycemia. This gene is a member of the 3-hydroxyacyl-CoA dehydrogenase gene family. The encoded protein functions in the mitochondrial matrix to catalyze the oxidation of straight-chain 3-hydroxyacyl-CoAs as part of the beta-oxidation pathway. Its enzymatic activity is highest with medium-chain-length fatty acids. Mutations in this gene cause one form of familial hyperinsulinemic hypoglycemia. The human genome contains a related pseudogene. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Entrez Gene record to access additional publications.
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Guanine nucleotide-binding proteins (G proteins) are involved as modulators or transducers in various transmembrane signaling systems. The G (i) proteins are involved in hormonal regulation of adenylate cyclase: they inhibit the cyclase in response to beta-adrenergic stimuli.
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Histones are basic nuclear proteins responsible for nucleosome structure of the chromosomal fiber in eukaryotes. Two molecules of each of the four core histones (H2A, H2B, H3, and H4) form an octamer, around which approximately 146 bp of DNA is wrapped in repeating units, called nucleosomes. The linker histone, H1, interacts with linker DNA between nucleosomes and functions in the compaction of chromatin into higher order structures. HIST1H1T is a member of the histone H1 family. Histones are basic nuclear proteins responsible for nucleosome structure of the chromosomal fiber in eukaryotes. Two molecules of each of the four core histones (H2A, H2B, H3, and H4) form an octamer, around which approximately 146 bp of DNA is wrapped in repeating units, called nucleosomes. The linker histone, H1, interacts with linker DNA between nucleosomes and functions in the compaction of chromatin into higher order structures. This gene is intronless and encodes a member of the histone H1 family. Transcripts from this gene lack polyA tails but instead contain a palindromic termination element. This gene is found in the large histone gene cluster on chromosome 6.
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Nucelobindin-2 (NUCB2; Nesfatin-1) was first isolated in adipocytes, but is also expressed by gastric mucosa and pancreatic beta cells. This pattern of nucleobindin-2 expression, as well as the presence of nucelobindin-2 within the plasma of rodents and humans, strongly suggests that this compound may act as a circulating regulatory factor. Nucelobindin-2 is reported to reduce food intake after administration. It is responsible for regulating appetite and production of body fat. Excess nucelobindin-2 in the brain leads to a loss of appetite, lack of nesfatin-1 in the brain leads to an increase of appetite.
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NPM3 is a member of Nucleophosmin (NPM) family. NPM is a ubiquitously expressed nucleolar phosphoprotein that continuously shuttles between the nucleus and cytoplasm
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Peroxisome proliferators include hypolipidemic drugs, herbicides, leukotriene antagonists, and plasticizers; this term arises because they induce an increase in the size and number of peroxisomes. Peroxisomes are subcellular organelles found in plants and animals which contain enzymes for respiration and for cholesterol and lipid metabolism. The action of peroxisome proliferators is thought to be mediated via specific receptors, called PPARs, which belong to the steroid hormone receptor superfamily. PPARs affect the expression of target genes involved in cell proliferation, cell differentiation and in immune and inflammation responses. Three closely related subtypes (alpha, beta/delta, and gamma) have been identified. This gene encodes the subtype PPAR-alpha, which is a nuclear transcription factor.
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GFI1 may be a transcription factor involved in regulating the expression of genes active in the S phase during cell cycle progression in T-cells. GFI1 may be involved in tumor progression. Defects in GFI1 are a cause of autosomal dominant severe congenital neutropenia (SCN) and dominant nonimmune chronic idiopathic neutropenia of adults (NI-CINA)
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De voorraad voor dit item is beperkt, maar kan beschikbaar zijn in een kortbijgelegen magazijn. Gelieve te controleren of u bent aangemeld op de site zodat de beschikbare voorraad weergegeven kan worden. Als het nog steeds zichtbaar is en u hulp nodig heeft, gelieve VWR te contacteren via 016/38 50 11/
Dit product is gemarkeerd als beperkt en kan enkel gekocht worden door goedgekeurde verzendingsaccounts. Als u hulp nodig heeft gelieve dan het VWR-Regelgevend Departement te contacteren via regulatory_affairs@vwr.com.
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Het originele artikel is niet langer beschikbaar. Het getoonde alternatief is wel beschikbaar.
Product(en) met dit symbool worden binnenkort niet meer verkocht - verkoop tot het einde voorraad. Alternatieven zijn mogelijk beschikbaar door te zoeken met het VWR artikelnummer dat hierboven wordt vermeld. Neem voor meer informatie contact op met onze Customer Service op 016 385 011.
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