Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Weitere Synonyme anzeigen
Wählen Sie die gewünschte Spezies
Human FCGR1A Protein expressed in Wheat germ - ABIN1353895
Sakamoto, Ito, Hatanaka, Soni, Mori, Sugimura: Discovery and characterization of a peptide motif that specifically recognizes a non-native conformation of human IgG induced by acidic pH conditions. in The Journal of biological chemistry 2009
High CD64 expression is associated with Mucosal Inflammation in Pediatric Crohn's Disease.
Expression of the Fc receptor CD64 on the surface of neutrophil granulocytes has been shown to correlate with complications in sepsis, infectious diseases ,and in solid organ transplanted patients.
The neutrophil/lymphocyte ratio is a better addition to C-reactive protein than CD64 index as a marker for infection in COPD.
FcgammaRI functions as a regulator for immune inflammation via acceleration of NF-kappaB regulating NLRP3 inflammasome signaling
HIV infection and HIV replication are associated with up-regulation of neutrophil CD64.
Neutrophil CD64 distinguished sepsis and non-septic ICU patients.
These results suggest that tyrosine phosphorylation may be critical in FcgammaRI-dependent endocytosis/phagocytosis that may be regulated by LILRB4 by triggering dephosphorylation of key signalling proteins.
neutrophil CD64 elevated in septic neonates
Neutrophil CD64 expression could be a good predictor as an immune parameter with high sensitivity and a negative predictive value for bacteremia in febrile neutropenic patients.
investigated consequences of 3 nonsynonymous SNPs for FcgammaRI; only SNP V39I reduces immune-complex binding of FcgammaRI whereas monomeric IgG binding is unaffected; SNPs I301M and I338T have no influence on monomeric IgG or immune complex binding, but FcRgamma signaling is decreased for both SNPs
Studies show that neutrophil CD64 (nCD64) is a reliable biomarker for diagnosing neonatal sepsis.
Data revealed that Erythema Nodosum Leprosum neutrophils express CD64, presumably contributing to the immunopathogenesis of the disease.
Our findings demonstrate that remarkable CD64 expression during Kawasaki dsease flare-ups may serve as a biomarker for diagnosis.
Both activation by Fcgamma-receptor (FcgammaR) dependent and independent stimuli were inhibited by inactive pepsin, indicating inhibition occurs in a downstream signaling pathway used for releasing granules.
FCGR1A expression is significantly upregulated in human masticatory mucosa during wound healing
This study demonstrated that CD64 discriminates between critically ill patients with culture positive and negative sepsis and correlates with severity of disease. However, CD64 index is not a good predictor for 28-day mortality in the critically ill patient.
CD64 seems to be a promising marker of infection in the intensive care setting, with Leuko64 showing a slight advantage
An elevated neutrophil CD64 index was a reliable prognostic biomarker for both short-term and long-term mortality in patients admitted for acute exacerbation of Chronic obstructive pulmonary disease.
Monocyte HLA-DR and neutrophil CD64 expression in critically ill infants with sepsis are related to age and infection.
The three-dimensional structure of a human IgG1 Fc fragment bound to wild-type human Fc-gamma RI is reported
FcgammaRI plays a role on macrophages to involve in renal inflammatory response, potentially via regulating the NLRP3 inflammasome-associated signaling.
FcgammaRI/FcgammaRIIB expression ratio in splenic macrophages was higher in the Treg-deficient immune thrombocytopenia (ITP) than in the Treg-deficient non-ITP and control mice
The IgG2 immune complexes activates osteoclastogenesis by binding to FcgammaRI.
Dbn1 regulates systemic anaphylaxis and IgE/Fcgr1-induced degranulation in mast cells by regulating actin reorganization and actin dynamics.
This study demonstrated that the activating FcgammaRs-mediated inflammation plays a critical role in anti-ganglioside Abs-induced neuropathy (injury to intact nerve fibers) in GBS.
N-glycans in FcgammaRIa interact with the OmpA of E. coli K1 for inducing disease pathogenesis
observations suggest that IgG-mediated inhibition of fibrocyte differentiation is mediated by FcgammaRs, with FcgammaRI mediating most of the signaling.
Inhibition of GCH1 prevented the Escherichia coli K1 induced expression of CD64 in macrophages in vitro and the development of bacteremia in a newborn mouse model of meningitis.
The PI3K inhibitor LY294002 inhibited BCR-mediated, but not TLR-mediated, induction of IkappaB-zeta, consistent with the role of PI3K in BCR signaling and its suppression by FcgammaR.
Dap12- and FcRgamma-deficiency exacerbates Granulocyte-Macrophage Colony-Stimulating Factor-driven monocyte differentiation and production of inflammatory monocyte-derived dendritic cells.
Tpl2 is activated by FcgammaR signals in macrophages and that its activation by these signals is required for ERK activation, cytoplasmic Ca(2+) influx, the induction of cytokine and coreceptor gene expression, and phagocytosis.
FcgammaRI partially mediates the protective effect of monoclonal antibody TA99 on metastatic melanoma tumor loads.
The mechanism(s) of phagocytosis in the second phase of blood incompatibility reaction required neither C3 nor FcgammaRs.
observations suggest that serum amyloid P, at least in part, uses FcgammaRI and FcRgamma to inhibit fibrocyte differentiation
CRP antagonism of eNOS is mediated by coupling of FcgammaRI to FcgammaRIIB by Src kinase and activation of inositol 5'-phosphatase 1, and consistent with this mechanism, both FcgammaRI and FcgammaRIIB are required for CRP to blunt endothelial repair in vivo.
IgG FcgammaRI (CD64) is a target of miR-127, as evidenced by reduced CD64 protein expression in macrophages overexpressing miR-127.
This review notes that the role of murine FcgammaRI differs considerably from human, based on sequence data, existence of the FcgammaRI variable region, and overview of disease models.
CD64 expression in macrophages is critical for the onset of meningitis by Escherichia coli K1.
Alveolar macrophages and Fc receptors (Fcgr1 and Fcgr3)-dependent elimination of influenza A virus-infected cells are essential for protection by influenza A virus anti-matrix protein 2 (M2) ectodomain IgG antibody.
This gene encodes a protein that plays an important role in the immune response. This protein is a high-affinity Fc-gamma receptor. The gene is one of three related gene family members located on chromosome 1.
Fc fragment of IgG, high affinity Ia, receptor for (CD64)
, Fc gamma receptor
, Fc-gamma RI
, Fc-gamma receptor I A1
, IgG Fc receptor I
, fc-gamma RIA
, high affinity immunoglobulin gamma Fc receptor I
, Fc fragment of IgG high affinity Ib receptor
, Fc fragment of IgG, high affinity Ib, receptor for (CD64)
, Fc receptor, IgG, high affinity I
, high affinity IgG Fc receptor, subunit beta
, high-affinity immunoglobulin gamma Fc receptor I
, IgG high affinity Fc receptor
, fc-gamma RI
, igG Fc receptor I
, FCGR1 variant 2
, FCGRI variant 1
, FCGRI variant 3