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Human CD55 Protein expressed in Human Cells - ABIN2002065
Bergelson, Chan, Solomon, St John, Lin, Finberg: Decay-accelerating factor (CD55), a glycosylphosphatidylinositol-anchored complement regulatory protein, is a receptor for several echoviruses. in Proceedings of the National Academy of Sciences of the United States of America 1994
Show all 5 Pubmed References
these data show a key role for HIF-1alpha (show HIF1A Proteins) in regulating the expression of CD55 on airway epithelium.
CD55 is produced by the synovium and deposited on local collagen fiber meshwork, where it protects against immune complex-mediated arthritis.
Fibrosis in Daf1-/- mice was accompanied by high expression of alpha-smooth muscle actin (show ACTG2 Proteins).
the downregulation of CD55 expression precedes, and has an important role regarding, the activation of C3 in the occurrence and development of DNP.
IFN-gamma (show IFNG Proteins)-producing NKT (show CTSL1 Proteins) cells enhance C5a generation via IL-10 (show IL10 Proteins)-mediated inhibition of CD55 expression on neutrophils, thereby exacerbating sepsis.
CD55 downregulates CD97 (show CD97 Proteins) surface expression on circulating leukocytes by a process that requires physical forces.
Trypanosoma cruzi-inoculated DAF-deficient mice provide a useful model for studying T-cell mediated immunity in skeletal muscle tissues.
Actively immunized experimental autoimmune myasthenia gravis mice deficient in either CD55 or CD59 (show CD59 Proteins) showed significant differences in adaptive immune responses and worsened disease outcome associated with increased levels of serum cytokines, modified production of acetylcholine receptor (show CHRNB1 Proteins) antibodies, and more complement deposition at the neuromuscular junction.
These data suggest that complement-independent interaction of CD55 with CD97 (show CD97 Proteins) is functionally relevant and involved in granulocyte homeostasis and host defense.
Complement dysregulation in the absence of CD55 provoked increased C3adesArg production that, in turn, caused altered lipid handling, resulting in atheroprotection and increased adiposity.
CD55 TT genotype was linked to H7N9/H1N1pdm09 influenza severity in a large Chinese cohort.
CD55 deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in CD55.
This study demonstrates an up-regulation of complement regulatory proteins, CD35 and CD55 in HIV associated pre-eclamptic compared to normotensive pregnancy.
There is an altered pattern of CD55 and CD59 (show CD59 Proteins) expression on RBCs (show SSU1 Proteins) of SCD (show SCD Proteins) Patients; however, it does not seem to play a causal role in the pathophysiology of anemia, and is unlikely to be influenced by the level of erythropoietin (show EPO Proteins) or other inflammatory mediators.
This study indicated that the CD97 (show CD97 Proteins) and CD55 proteins might be reliable biomarkers to predict the metastasis status and prognosis of intrahepatic cholangiocarcinoma patients.
Expression of PBMC-DAF declined in patients both at mRNA and surface level and correlated negatively with the disease activity. Expression of IFN-gamma (show IFNG Proteins) also declined in patients but correlated positively with DAF and negatively with disease activity
Over expression of CD55 in brushing samples taken from Barrett's esophagus
present study suggested that the expressions of CD97 antigen (show CD97 Proteins) and decay accelerating factor DAF were both upregulated in human cervical squamous cell carcinoma
conclude that CD55 expression is affected by glycemic status in human islets and plays a critical role in maintaining the conserved structure of rafts in pancreatic islets, which is similar to that of the related complement inhibitor CD59 (show CD59 Proteins)
CD55 is an essential host factor for P. falciparum invasion. CD55-null erythrocytes were refractory to invasion by all isolates of P. falciparum because parasites failed to attach properly to the erythrocyte surface.
This gene encodes a protein involved in the regulation of the complement cascade. The encoded glycoprotein is also known as the decay-accelerating factor (DAF)\; binding of DAF to complement proteins accelerates their decay, disrupting the cascade and preventing damage to host cells. Antigens present on the DAF glycoprotein constitute the Cromer blood group system (CROM). Two alternatively spliced transcripts encoding different proteins have been identified. The predominant transcript encodes a membrane-bound protein expressed on cells exposed to plasma component proteins but an alternatively spliced transcript produces a soluble protein present at much lower levels. Additional, alternatively spliced transcript variants have been described, but their biological validity has not been determined.
CD55 molecule, decay accelerating factor for complement (Cromer blood group)
, complement decay-accelerating factor
, decay-accelerating factor (GDab-TCS)
, Cromer blood group
, GPI anchor addition signal
, complement decay-accelerating factor, GPI-anchored
, decay accelerating factor 1
, CD55 antigen
, complement decay-accelerating factor transmembrane isoform