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Validated All-in-One™ qPCR Primer for CD59(NM_203330.2) Search again
Product ID:
HQP054719
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
16.3A5, 1F5, EJ16, EJ30, EL32, G344, HRF-20, HRF20, MAC-IP, MACIF, MEM43, MIC11, MIN1, MIN2, MIN3, MIRL, MSK21, p18-20
Gene Description:
CD59 molecule (CD59 blood group)
Target Gene Accession:
NM_203330.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes a cell surface glycoprotein that regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the assembly of this complex, thereby inhibiting the incorporation of multiple copies of C9 into the complex, which is necessary for osmolytic pore formation. This protein also plays a role in signal transduction pathways in the activation of T cells. Mutations in this gene cause CD59 deficiency, a disease resulting in hemolytic anemia and thrombosis, and which causes cerebral infarction. Multiple alternatively spliced transcript variants, which encode the same protein, have been identified for this gene. [provided by RefSeq].
Gene References into function
- The complement inhibitor CD59 and the lymphocyte function-associated antigen-3 (LFA-3, CD58) genes possess functional binding sites for the p53 tumor suppressor protein.
- Antigen-presenting cell exosomes are protected from complement-mediated lysis by expression of CD55 and CD59.
- CD59 is an adaptor for ecto-calreticulin in neutrophils
- Although CD55 and CD59 deficiency in primary or secondary AIHA, it appears that this defect plays a facilitator rather than a triggering role for the hemolytic process.
- CD59 is physically associated with NKp46 and NKp30 and activate human nk cell-mediated cytotoxicity.
- Complement regulatory proteins such as MCP and CD59 are expressed in the human and wild-type embryonic brain.
- Presence of CD59 on Purkinje cells at various levels in eight of 14 cases with no cerebellar pathology suggests that Purkinje cells not expressing CD59 could be especially prone to complement-mediated damage.
- Significant difference in intensity of the staining of CD55 and CD46 among cells in various layers of normal esophageal mucosa and esophageal carcinoma cells, but not in the staining of CD59.
- During respiratory syncytial virus assembly in Hep2 cells, the cellular distribution of the complement regulatory protein, CD59 changes and high levels of this cellular protein are incorporated into mature virus filaments.
- Prostasomes from cancer cells had higher expression of CD59 than those of normal cells.
- Glycation inactivation of hCD59 leads to increased membrane attack complex deposition may contribute to the extensive vascular pathology that complicates human diabetes.
- Streptococcus intermedius intermedilysin specifically binds to huCD59 via residues that are the binding site for the C8alpha and C9 complement proteins
- CD55-CD59- deficient granulocytes and red blood cells predicts responsse to immunosuppressive agents in aplastic anemia.
- CD59 on target cells enhances the cytotoxicity of natural killer cells, an effect dependent on the glycosylphosphatidylinositol anchor in CD59.
- analysis of the CD59-C9 binding interaction
- Upregulation of CD59 and decay-accelerating factor by atorvastatin in hypoxia prevented deposition of C3, C9 and cell lysis that follows exposure of reoxygenated vascular endothelial cells to serum.
- CD55/59 deficiency in Campath-treated patients with paroxysmal nocturnal hemoglobinuria msay indicate that deficiency could predispose to a complication of this immunosuppressive therapy.
- HHV-7 infection causes elevation of the CRPs CD46 and CD59, which may be a possible mechanism for HHV-7 to evade humoral immunity via complement.
- When compared with previous models of CD59 determined using NMR, some interesting differences are noted, including the position of helix alpha1, which contributes to the binding surface for C8 and C9.
- These results suggest that IRE1alpha-mediated mRNA cleavage functions even in mammals as a common system to regulate gene expression.
- Essential for the protection of neurons in the NT2-N teratocarcinoma cell line against complement attack.
- the amount of C5b-9-AF488 bound to K562 cells after complement activation was highly heterogeneous and inversely correlated with the CD59 level of expression
- Electron-density map of recombinant CD59 crystals shows an as yet unidentified small molecule in the predicted C8/C9-binding site.
- Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by absence of CD59 from the surface of affected granulocytes.
- up-regulation of CD59 via ERK5/KLF2 activation leads to endothelial resistance to complement-mediated injury and protects from atherogenesis in regions of laminar shear stress
- erythrocytes are deficient in CD55 and/or CD59 in HIV patients
- Results indicate that W40 of human CD59 is important to its activity, and prohibition of this site may be a potential way to increase complement activity and to treat tumors
- Adenovirus-mediated delivery of hCD59 to retinal pigment epithelium, or cornea culturee protects these cells from membrane attach comlpex-mediated ddamage.
- Expression levels of CD47, CD35, CD55, and CD59 on red blood cells and signal-regulatory protein-alpha,beta on monocytes from patients with warm autoimmune hemolytic anemia.
- In prostate cancer cells in culture, delta-catenin was co-localized with caveolin-1 and CD59, suggesting its potential excretion into extracellular milieu through exosome/prostasome associated pathways.
- Complement regulator CD59 protects against atherosclerosis by restricting the formation of complement membrane attack complex.