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anti-Human C9 Anticorps:
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Human Monoclonal C9 Primary Antibody pour WB - ABIN532660
Klegeris, Schwab, Bissonnette, McGeer: Induction of complement C9 messenger RNAs in human neuronal cells by inflammatory stimuli: relevance to neurodegenerative disorders. dans Experimental gerontology 2001
Show all 3 Pubmed References
Mouse (Murine) Polyclonal C9 Primary Antibody pour ICC, IHC - ABIN5013382
Fu, Ju, Lin, Xiao, Li, Zhuang, Zhang, Ma, Li, Ma, Su, Wang, Qin, Liang: Target deletion of complement component 9 attenuates antibody-mediated hemolysis and lipopolysaccharide (LPS)-induced acute shock in mice. dans Scientific reports 2016
Human Monoclonal C9 Primary Antibody pour FACS, IA - ABIN4299956
Hatanaka, Seya, Yoden, Fukamoto, Semba, Inai: Analysis of C5b-8 binding sites in the C9 molecule using monoclonal antibodies: participation of two separate epitopes of C9 in C5b-8 binding. dans Molecular immunology 1992
Human Polyclonal C9 Primary Antibody pour ICC, IF - ABIN4299957
Neiman, Fredolini, Johansson, Lehtiö, Nygren, Uhlén, Nilsson, Schwenk: Selectivity analysis of single binder assays used in plasma protein profiling. dans Proteomics 2013
Human Polyclonal C9 Primary Antibody pour ICC, IF - ABIN4299959
Halfter, Moes, Asgeirsson, Halfter, Oertle, Melo Herraiz, Plodinec, Jenoe, Henrich: Diabetes-related changes in the protein composition and the biomechanical properties of human retinal vascular basement membranes. dans PLoS ONE 2018
Human Monoclonal C9 Primary Antibody pour ELISA - ABIN2477820
Huang, Qiao, Abagyan, Hazard, Tomlinson: Defining the CD59-C9 binding interaction. dans The Journal of biological chemistry 2006
The data supports the assumption that C9 gene expression may stimulate the expression of inflammatory (NLRP3) and angiogenic growth factors (VEGF) in retinal pigment epithelial cells.
Serum-expressed apolipoprotein B-100 protein, C9 Complement, and gelsolin can be used for differential diagnosis of Barrertts esophagus and adenocarcinoma of esophagus.
Patients with advanced atrophic AMD carried these rare variants more frequently than patients with neovascular AMD (11 of 93 [11.8%] vs 40 of 835 [4.8%]; P = .04).
Complement C5b-9 complex sensitizes 661W photoreceptor cells to both apoptosis and necroptosis.
Data indicate that complement C9 binds to the ATPase domain of mortalin.
Borrelial CspA binds the human terminal complement components C7 and C9 and blocks assembly and membrane insertion of the terminal complement complex (TCC).
Liver biopsy specimens from chronically hepatitis C virus-infected patients exhibited a lower level of C9 mRNA expression than liver biopsy specimens from unrelated disease or healthy control human liver RNA.
Caveolin-1 and dynamin-2 are essential for removal of the complement C5b-9 complex via endocytosis.
the haploinsufficiency of C9, a terminal complement complex component, engenders reduced intraocular secretion of VEGF and decreased risk for CNV development.
C9 and fucosylated form could serve as a useful marker for SQLC.
It was concluded that variations in the complement component 9 gene are unlikely to influence clearance of chronic hepatitis B virus infection and hepatocellular carcinoma occurrence.
Mapping the intermedilysin-human CD59 receptor interface reveals a deep correspondence with the binding site on CD59 for complement binding proteins C8alpha and C9.
These results suggested that the lack of membrane attack complex because of an Arg95Stop mutation of the complement component 9 gene predisposed patients to pathognomonic glomerulonephritis.
Complement C5b-9 induce a JNK/Bid-dependent and JNK-independent necrotic cell death.
Data show that C1q, C4, C3, and C9 bind to thrombin receptor-activating peptide-activated platelets in lepirudin-anticoagulated platelet-rich plasma (PRP) and whole blood.
provided evidence for the recognition of membrane-bound C9 on complement-lysed ghosts by an antibody specific for the helix-turn-helix fold.
Data show that mortalin supports cancer cell resistance to complement-dependent cytotoxicity and suggest consideration of mortalin as a novel target for cancer adjuvant immunotherapy.
The human complement C9 gene: structural analysis of the 5' gene region and genetic polymorphism studies.
C9 binding is dependent on the N-terminal modules (thrombospondin type 1 and low-density lipoprotein receptor class A) of C8 alpha together with the C8 alpha membrane attack complex/perforin domain.
Founder effect was demonstrated for the R95X mutation of the C9 gene in Japanese
Results determined the 2.2 A crystal structure of monomeric Complement component 9 (C9) and the 3.9 A resolution cryoelectron microscopy structure of C9 in a polymeric assembly.
these results not only confirm the critical role of C5b-9 in complement-mediated hemolysis and but also highlight the critical role of C5b-9 in inflammasome activation.
This gene encodes the final component of the complement system. It participates in the formation of the Membrane Attack Complex (MAC). The MAC assembles on bacterial membranes to form a pore, permitting disruption of bacterial membrane organization. Mutations in this gene cause component C9 deficiency.
complement component C9
, complement protein C9
, complement component 9 L homeolog