| Description | DNAJC7 Human Pre-designed siRNA Set A contains three designed siRNAs for DNAJC7 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control. Components DNAJC7 siRNA-1: 5 nmol (HPLC) DNAJC7 siRNA-2: 5 nmol (HPLC) DNAJC7 siRNA-3: 5 nmol (HPLC) siRNA Negative DNAJC7 Human Pre-designed siRNA Set A contains three designed siRNAs for DNAJC7 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control. Components DNAJC7 siRNA-1: 5 nmol (HPLC) DNAJC7 siRNA-2: 5 nmol (HPLC) DNAJC7 siRNA-3: 5 nmol (HPLC) siRNA Negative Control: 5 nmol (HPLC) FAM-labeled siRNA Negative Control: 5 nmol (HPLC) GAPDH siRNA Positive Control:5 nmol (HPLC)... Read More | Inquire | Purity:>95%, by SDS-PAGE visualized with Coomassie® Blue Staining.Description：CD200 R1, also known as OX-2 receptor, is a 90 kDa transmembrane protein in the immunoglobulin superfamily and is important in the regulation of myeloid cell activity. The human CD200 R1 cDNA encodes a 325 Purity:>95%, by SDS-PAGE visualized with Coomassie® Blue Staining.Description：CD200 R1, also known as OX-2 receptor, is a 90 kDa transmembrane protein in the immunoglobulin superfamily and is important in the regulation of myeloid cell activity. The human CD200 R1 cDNA encodes a 325 amino acid (aa) precursor that includes a 28 aa signal sequence, a 215 aa extracellular domain (ECD), a 21 aa transmembrane segment, and a 61 aa cytoplasmic domain. The ECD is composed of one Ig-like V-type domain and one Ig-like C2-type domain. Within the ECD, human CD200 R1 shares 56% aa sequence identity with both mouse and rat CD200 R1. Alternate splicing of the human CD200 R1 mRNA generates four isoforms, two of which are truncated in the Ig-C2 domain and are likely secreted. In human, a separate CD200 RL gene encodes a protein that shares 81% ECD aa identity with CD200 R1. In mouse, at least four genes for CD200 R1-like molecules have been described. CD200 R1 expression is restricted primarily to mast cells, basophils, macrophages, and dendritic cells, while its ligand, CD200, is widely distributed. Disruption of this receptor-ligand system by knockout of the CD200 gene in mice leads to increased macrophage number and activation and predisposition to autoimmune disorders. Association of CD200 with CD200 R1 takes place between their respective N-terminal Ig-like domains. The capacity of CD200 R1-like molecules to interact with CD200 is controversial. CD200 R1 propagates inhibitory signals despite lacking a cytoplasmic ITIM (immunoreceptor tyrosine-based inhibitory motif). CD200 R1-like molecules, in contrast, are potentially activating receptors by means of their association with DAP12. CD200R1 signaling inhibits the expression of proinflammatory molecules including TNFs, IFNs, and inducible nitric oxide synthase in response to selected stimuli, which implicate that CD200/CD200R1 inhibitory signaling pathway plays a prominent role in limiting inflammation in a wide range of inflammatory diseases. Furthermore, the CD200/CD200R inhibitory signaling constitutes one of the most suitable endogenous immunoregulatory molecule candidate to restore the immune suppressive status of the CNS altered in chronic neuroinflammatory situations... Read More | Purity>97% SDS-PAGE and HPLC analyses. FunctionLA-PF4 stimulates DNA synthesis, mitosis, glycolysis, intracellular cAMP accumulation, prostaglandin E2 secretion, and synthesis of hyaluronic acid and sulfated glycosaminoglycan. It also stimulates the formation and secretion of plasminogen Purity>97% SDS-PAGE and HPLC analyses. FunctionLA-PF4 stimulates DNA synthesis, mitosis, glycolysis, intracellular cAMP accumulation, prostaglandin E2 secretion, and synthesis of hyaluronic acid and sulfated glycosaminoglycan. It also stimulates the formation and secretion of plasminogen activator by human synovial cells. NAP-2 is a ligand for CXCR1 and CXCR2, and NAP-2, NAP-2(73), NAP-2(74), NAP-2(1-66), and most potent NAP-2(1-63) are chemoattractants and activators for neutrophils. TC-1 and TC-2 are antibacterial proteins, in vitro released from activated platelet alpha-granules. CTAP-III(1-81) is more potent than CTAP-III desensitize chemokine-induced neutrophil activation.Post-translationalProteolytic removal of residues 1-9 produces the active peptide connective tissue-activating peptide III (CTAP-III) (low-affinity platelet factor IV (LA-PF4)). Proteolytic removal of residues 1-13 produces the active peptide beta-thromboglobulin, which is released from platelets along with platelet factor 4 and platelet-derived growth factor. NAP-2(1-66) is produced by proteolytical processing, probably after secretion by leukocytes other than neutrophils. NAP-2(73) and NAP-2(74) seem not be produced by proteolytical processing of secreted precursors but are released in an active form from platelets... Read More | Purity:>95%, by SDS-PAGE visualized with Coomassie® Blue Staining. Description： Neuron specific enolase (NSE), also known as ENO2 or gamma-enolase, is a dimeric, Mg2+-dependent enzyme that catalyzes the dehydration of 2-phospho-D glycate (PGA) to phosphoenolpyruvate (PEP) in the Purity:>95%, by SDS-PAGE visualized with Coomassie® Blue Staining. Description： Neuron specific enolase (NSE), also known as ENO2 or gamma-enolase, is a dimeric, Mg2+-dependent enzyme that catalyzes the dehydration of 2-phospho-D glycate (PGA) to phosphoenolpyruvate (PEP) in the glycolytic pathway and catalyzes the reverse reaction in gluconeogenesis. There are three major isozymes of enolase expressed in selective vertebrate tissues from separate genes: alpha (ENO1), beta (ENO3), and gamma (ENO2). NSE is a highly expressed, specific neuron isozyme making it a useful marker for tumors derived from neuronal cells. Neuron-specific enolase is implicated as a diagnostic and prognostic marker in numerous diseases including early small cell lung cancer, prostate cancer, multiple myeloma, traumatic brain injury, acute spinal cord injury, acute ischemic stroke, and post-concussion symptoms. NSE expression and activity are increased in neuronal and glial activation and injury, risk factors implicated in neurodegenerative disease. Elevation of NSE promotes glycolysis, proliferation, activation and migration through its C-terminus to activate PI3K and MAPK signal transduction pathways while inhibition of enolase has been shown to attenuate inflammatory events. NSE can be regulated through cleavage of the C-termini by cathepsin X or inhibited directly by antibiotic SF2312. Inhibition has been proposed as a therapeutic strategy in cancer... Read More |