"Bioss"

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Involved in the maintenance and repair of the intestinal mucosa. Promotes the mobility of epithelial cells in healing processes (motogen).

Supplier: Bioss

Glutamate receptors mediate most excitatory neurotransmission in the brain and play an important role in neural plasticity, neural development and neurodegeneration. Ionotropic glutamate receptors are categorized into NMDA receptors and kainate/AMPA receptors, both of which contain glutamate-gated, cation-specific ion channels. Kainate/AMPA receptors are co-localized with NMDA receptors in many synapses and consist of seven structurally related subunits designated GluR-1 to -7. The kainate/AMPA receptors are primarily responsible for fast excitatory neurotransmission by glutamate, whereas the NMDA receptors exhibit slow kinetics of Ca2+ ions and a high permeability for Ca2+ ions.

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The downstream regulatory element, DRE, acts as a location-dependent gene silencer. DREAM (for DRE-antagonist modulator) is a Ca2+-regulated transcriptional repressor that specifically binds to the DRE. DREAM regulates transcription of prodynorphin and c-Fos genes and shows 99% nucleotide homology to the Kv channel-interacting proteins (KChIPs). KChIP family members include KChIP1, which is expressed in brain, KChIP2, which is expressed in heart, brain, and lung, KChIP3 (also designated calsenilin), which is expressed in brain and testis and KChIP4.

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ZNF431 belongs to the krueppel C2H2-type zinc-finger protein family and is probably involved in transcriptional regulation.

Supplier: Bioss

Mediates interactions of advanced glycosylation end products (AGE). These are nonenzymatically glycosylated proteins which accumulate in vascular tissue in aging and at an accelerated rate in diabetes. Acts as a mediator of both acute and chronic vascular inflammation in conditions such as atherosclerosis and in particular as a complication of diabetes. AGE/RAGE signaling plays an important role in regulating the production/expression of TNF-alpha, oxidative stress, and endothelial dysfunction in type 2 diabetes. Interaction with S100A12 on endothelium, mononuclear phagocytes, and lymphocytes triggers cellular activation, with generation of key proinflammatory mediators. Interaction with S100B after myocardial infarction may play a role in myocyte apoptosis by activating ERK1/2 and p53/TP53 signaling (By similarity). Receptor for amyloid beta peptide. Contributes to the translocation of amyloid-beta peptide (ABPP) across the cell membrane from the extracellular to the intracellular space in cortical neurons. ABPP-initiated RAGE signaling, especially stimulation of p38 mitogen-activated protein kinase (MAPK), has the capacity to drive a transport system delivering ABPP as a complex with RAGE to the intraneuronal space. Can also bind oligonucleotides.

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High-affinity self-ligand important in bidirectional T-cell to B-cell stimulation. SLAM-induced signal-transduction events in T-lymphocytes are different from those in B-cells. Two modes of SLAM signaling are likely to exist: one in which the inhibitor SH2D1A acts as a negative regulator and another in which protein-tyrosine phosphatase 2C (PTPN11)-dependent signal transduction operates.

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The JNK-interacting protein (JIP) group of scaffold proteins selectively mediates JNK signaling by aggregating specific components of the MAPK cascade to form a functional JNK signaling module. Required for JNK activation in response to excitotoxic stress. Cytoplasmic MAPK8IP1 causes inhibition of JNK-regulated activity by retaining JNK in the cytoplasm and inhibiting JNK phosphorylation of c-Jun. May also participate in ApoER2-specific reelin signaling. Directly, or indirectly, regulates GLUT2 gene expression and beta-cell function. Appears to have a role in cell signaling in mature and developing nerve terminals. May function as a regulator of vesicle transport, through interactions with the JNK-signaling components and motor proteins (By similarity). Functions as an anti-apoptotic protein and whose level seems to influence the beta-cell death or survival response.

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The steady state of protein tyrosyl phosphorylation in cells is regulated by the opposing action of tyrosine kinases and protein tyrosine phosphatases (PTPs). Several groups have independently identified a non transmembrane PTP, designated SHPTP1 (also known as PTP1C, HCP and SHP), which is primarily expressed in hematopoietic cells and characterized by the presence of two SH2 domains N terminal to the PTP domain. A second and much more widely expressed PTP with SH2 domains, SHPTP2 (also designated PTP1D and Syp), has been identified. SHP2 is a protein tyrosine phosphatase that is widely expressed and plays a regulatory role in various cell signaling events that are important for many cell functions, such as mitogenic activation, metabolic control, transcription regulation, and cell migration.

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Anti-ADAR Rabbit Polyclonal Antibody

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GPR10.

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ADAR1 converts adenosine to inosine in dsRNA, which destabilizes the dsRNA helix. This activity is important for various functions like site-specific RNA editing of transcripts of the glutamate receptors and modifying viral RNA genomes (which may be responsible for hypermutation of certain negative-stranded viruses, e.g., measles virus). ADAR1 also binds to short interfering RNAs (siRNA) without editing them and suppresses siRNA-mediated RNA interference. This protein is ubiquitously expressed, with the highest levels being found in brain and lung.

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5-aminolevulinate synthase 1 (ALAS-H) and 2 (ALAS-E) are two isoforms of ALAS, an enzyme catalyzing the first step of the heme biosynthetic pathway in mammals. The erythroid-specific isoenzyme, ALAS-E, regulates the first step of hematopoietic cell differentiation and iron metabolism in the liver. ALAS-H is a housekeeping protein which mediates synthesis of early heme in the mitochondria of most cells. Succinyl CoA associates with ALAS-E in protein conformation change and translocation of ALAS-E into the mitochondria and does not interact with ALAS-H. The ALAS-E 5'-flanking region contains binding sites for nuclear activators such as GATA-1, NF-E2 and EKLF. Since the ALAS gene maps to the X chromosome, mutation of the gene leads to the pyridoxine-refractory X-linked sideroblastic anemia.

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CCDC94

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NHLRC3 contains 4 NHL repeats. The function of the NHLRC3 protein remains unknown. Key tumor suppressor genes on chromosome 13 include the breast cancer susceptibility gene, BRCA2, and the RB1 (retinoblastoma) gene. RB1 encodes a crucial tumor suppressor protein which, when defective, leads to malignant growth in the retina and has been implicated in a variety of other cancers. The gene SLITRK1, which is associated with Tourette syndrome, is on chromosome 13. As with most chromosomes, polysomy of part or all of chromosome 13 is deleterious to development and decreases the odds of survival. Trisomy 13, also known as Patau syndrome, is quite deadly and the few who survive past one year suffer from permanent neurologic defects, difficulty eating and vulnerability to serious respiratory infections.

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CHPT1, also known as AAPT1-like protein and Diacylglycerol cholinephosphotransferase 1, is a 406 amino acid multi-pass membrane protein that is localised to the golgi apparatus. By catalyzing the phosphatidylcholine biosynthesis from CDP-choline, it plays an essential role in the formation and maintenance of vesicular membranes. CHPT1 is most abundant in testis, as well as small intestine, heart, colon, spleen and prostate. Expression of CHPT1 is increased in cancerous breast cells as compared to normal breast cell lines and it has been determined that the CHPT1 gene exhibits mutations within the cancerous cells. Interestingly, exposure to mustard gas significantly decreases CHPT1 gene expression and activity, an event that may play an important role in the development of acute respiratory distress syndrome (ARDS). There are two isoforms of CHPT1 that are produced as a result of alternative splicing events.

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Voltage-sensitive calcium channels (VSCC) mediate the entry of calcium ions into excitable cells and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and cell death. The isoform alpha-1G gives rise to T-type calcium currents. T-type calcium channels belong to the "low-voltage activated (LVA)" group and are strongly blocked by mibefradil. A particularity of this type of channels is an opening at quite negative potentials and a voltage-dependent inactivation. T-type channels serve pacemaking functions in both central neurons and cardiac nodal cells and support calcium signaling in secretory cells and vascular smooth muscle. They may also be involved in the modulation of firing patterns of neurons which is important for information processing as well as in cell growth processes. There are 2 isoforms of CACNA1H and 14 isoforms if CACNA1G, produced by alternative splicing.