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Human MBL2 Protein expressed in CHO Cells - ABIN2002787
Super, Gillies, Foley, Sastry, Schweinle, Silverman, Ezekowitz: Distinct and overlapping functions of allelic forms of human mannose binding protein. dans Nature genetics 1993
Show all 6 Pubmed References
Damaging nonsense variants of African ancestry in the DEFB1 and MBL2 genes that encode anti-microbial proteins that presumably defend the fetal membranes from infectious agents confer risk of preterm premature rupture of membranes and preterm birth in African Americans.
Our results suggest that binding capacity of MBL could be an indicator of clinical manifestation in Chronic Chagas cardiomyopathy.
Serum mannose-binding lectin (MBL) and MBL genotypes do not determine the risk for developing febrile neutropenia (FN).
MBL may play a role in modulating host immunity, persistence of Hepatitis C and disease progression
MBL -550, -221 and exon 1 polymorphisms, can be related to the development clinical manifestations caused by HHV-8, especially in HIV/HHV-8 coinfected patients who present the intermediate expression haplotypes of MBL.
Mannose-Binding Lectin-Deficient Donors Increase the Risk of Bacterial Infection and Bacterial Infection-Related Mortality After Liver Transplantation
C1q binding to CR1 shares with MBL a main common interaction site on the collagen stalks but also subsidiary sites most probably located on C1q globular heads, contrarily to MBL.
Studied the structural and functional changes of genetic variants of Mannose-Binding Lectin 2 (MBL2) and myelin protein zero (MPZ) in Colombian families with leprosy.
This study demonstrates that the MBL2/rs1800450 and KLRC4/rs2617170 are susceptibility factors for Behcet's disease in a Chinese Han population.
These findings suggest that high activity of the classical complement pathway, and MBL deficiency, might be associated with an increased odds of unprovoked venous thromboembolism, independent of activation of Tissue Factor-induced coagulation.
he carrying of MBL2 exon 1 codon 54 variant allele (B) was shown to be a risk factor for Recurrent vulvovaginal candidiasis in childbearing women.
Positive correlation of MBL levels with anti-ds DNA titers in systemic lupus erythematosus suggest that its values vary with activity and could be a potential biomarker of the disease.
The -221G>C polymorphism of MBL2, the -159C>T polymorphism of CD14 and the TNF-857 polymorphism of TNF-a are risk factors for spinal spinal tuberculosis (TB) and may be involved in the development of spinal TB in the Chinese population. These factors are indicators of susceptibility to spinal TB and require clinical attention.
MBL2 protein blood level was significantly reduced in the hepatocellular carcinoma patients.The association in MBL2 polymorphisms and the risk of hepatocellular carcinoma.
Results suggested the involvement of MBL2 (rs1800450) polymorphism and its protein in rheumatic heart disease pathogenesis.
MBL deficiency was significantly more frequent in the juvenile idiopathic arthritis Yersinia-reactive antibodies-positive group than in patients without Yersinia-reactive antibodies or in controls
it can be concluded that molecular analysis of MBL rs1800450 AA genotype and TNF-alpha rs1800620 AA genotype is important in the early detection and treatment of T2DM with H. pylori cagA(+) infection.
The results suggest that MBL deficiency and the presence of MBL2 gene polymorphisms that lead to MBL deficiency are risk factors for the occurrence of miscarriage in patients with RA.
These results suggest that the MBL2 gene Codon 54 and TNF-alpha gene G308A polymorphisms are not associated with an increased risk for development of tuberculosis in our patients.
Studies results provide evidence that Crohn's disease patients have an impairment in mannose-binding lectin-mannose-associated serine protease functional activity and that this defect is associated with mannose-binding lectin 2 and NOD2 variants.
MBL2 polymorphisms were associated with some disease groups and with the presence of some etiologic agents
MBL1 was also found to be expressed in the lung, testis and brain, whereas low expression of MBL2 was detected in the testis and kidney.
Single nucleotide polymorphisms in MBL2 at exon 1 were detected using polymerase chain reaction single-strand conformation polymorphism analysis and DNA sequencing techniques in 825 Chinese Holstein cows.
the relationship between the variants of the bovine MBL2 gene and milk production traits, mastitis, serum MBL-C levels and hemolytic complement activity in both classical pathway (CH50) and alternative pathway (ACH50) in Chinese Holstein cattle
this study shows that MBL-C expression is induced in the gut in response to Candida albicans sensing and is required for intestinal homeostasis and host defense against Candida albicans
Targeted deletion of Mbl1/2 causes differential levels of inflammation-related gene sets at baseline and after exposure to ozone and significantly reduces pulmonary inflammation, thus indicating an important innate immunomodulatory role of the Mbl1/2 genes.
Human and murine data together indicate that SP-A, SP-D and MBL are synthesized in early gestational tissues, and may contribute to regulation of immune response at the feto-maternal interface during pregnancy.
These data show that modulation of MBL is involved in the protection against renal I/RI induced by dietary restriction, and suggest that the mechanisms of protection induced by dietary restriction and fasting may be different.
ALI in H5N1-infected mice was caused by excessive complement activation, as demonstrated by deposition of C3, C5b-9, and MBL-C in lung tissue, and by up-regulation of MBL-associated serine protease-2 and the complement receptors C3aR and C5aR.
demonstrate that apolipoprotein E (Apoe), mannose-binding lectin 2 (Mbl2), and parotid secretory protein (Psp) are present at significantly different quantities in depleted plasma of diabetic NZO mice compared to non-diabetic controls
Data indicate that no change of mannan-binding lectin MBL-A during the study, however, mannan-binding lectin MBL-C concentration increased in median by 3.6-fold (2.9; 4.5-fold) during the study in the diabetic group.
These observations point to a previously unappreciated role for MBL in regulating host resistance and cardiac inflammation during infection with a major human pathogen.
MBL plays a key role in clearing influenza A virus and maintaining lung homeostasis.
Data show that genetically defined MBL-deficiency is associated with a better outcome after acute stroke.
Recombinant mouse ficolin A, mannose-binding lectin-A, and mannose-binding lectin-C bound to fibrinogen in a dose-dependent manner. The lectin pathway, through mannose-binding lectins, synchronized with blood coagulation.
present in the decidua in abortion-prone mating combinations
selectively expressed in villous epithelial cells of the small intestine
role for MBL in clearance of dying cells
exposure of MBL to Kupffer cells increased cell surface SR-A expression and phagocytosis of S. aureus and E. coli; and MBL bound to lipid A, LPS, and S. aureus
MBL as an important molecule in the maintenance of the homeostatic balance in the skin
both the presence of capsule and wild-type cell wall architecture preclude MBL binding to C. neoformans.
MBL deficiency increases susceptibility to controlled cortical impact through C3-independent mechanisms
The in vitro binding and activation of the human and mouse complement systems was analysed and the susceptibility to infection in complement-deficient mouse strains, was tested.
These model studies have uncovered unexpected roles of MBL and evidence of its interaction with other molecules of the innate immune system.
MBL binding can be inhibited by at least two separate and independent mechanisms.
report multiple copies of MBL-like genes, with up to three copies tightly linked within a cluster spanning approximately 15 kb on chromosome 2
This gene encodes the soluble mannose-binding lectin or mannose-binding protein found in serum. The protein encoded belongs to the collectin family and is an important element in the innate immune system. The protein recognizes mannose and N-acetylglucosamine on many microorganisms, and is capable of activating the classical complement pathway. Deficiencies of this gene have been associated with susceptibility to autoimmune and infectious diseases.
, mannan-binding lectin
, mannose-binding lectin (protein C) 2, soluble (opsonic defect)
, mannose-binding lectin 2, soluble (opsonic defect)
, mannose-binding protein C
, 27 kDa mannan-binding protein monomeric subunit
, mannose-binding lectin 2, soluble
, Mannose-binding protein C
, c-type lectin
, mannose binding lectin, liver (A)
, mannose-binding lectin 2
, soluble mannose-binding lectin
, mannan-binding protein
, RA-reactive factor P28A subunit
, mannose binding lectin 2 (protein C)
, mannose-binding protein C (liver)
, ra-reactive factor polysaccharide-binding component p28A
, raRF p28A
, mannose binding lectin (C)
, mannose binding lectin, liver (C)
, mannose-binding lectin (protein C) 2, soluble
, Mannan-binding protein
, Mannose-binding lectin
, hexose-binding lectin 3
, mannose binding lectin 2
, mannose binding-like lectin