Ignet

Gene Information

Gene symbol: MBL2

Gene name: mannose-binding lectin (protein C) 2, soluble

HGNC ID: 6922

Synonyms: COLEC1

Related Genes

#	Gene Symbol	Number of hits
1	ADIPOQ	1 hits
2	BUD31	1 hits
3	CCR5	1 hits
4	CD14	1 hits
5	CD244	1 hits
6	CD4	1 hits
7	CFH	1 hits
8	CRP	1 hits
9	CXCR4	1 hits
10	FCAMR	1 hits
11	FCN1	1 hits
12	FCN2	1 hits
13	FCN3	1 hits
14	IL10	1 hits
15	IL18	1 hits
16	IL1B	1 hits
17	IL4	1 hits
18	IL8	1 hits
19	KLRG1	1 hits
20	LOH19CR1	1 hits
21	MASP1	1 hits
22	MASP2	1 hits
23	PMP2	1 hits
24	SFTPA1	1 hits
25	SFTPD	1 hits
26	TLR2	1 hits
27	TNF	1 hits

Related Sentences

#	PMID	Sentence
1	455286	Adriamycin and cyclophosphamide treatment of BALB/c x DBA/2F1 mice were studied alone and in combination with immunotherapeutic agents, pyran copolymer and Bacillus Calmette-Guérin, on macrophage cytotoxic ability, As assessed by direct viable cell counts of MBL-2 leukemia cells, both Adriamycin and cyclophosphamide produced growth-inhibitory macrophages.
2	9300722	Induction of TNF-alpha in human peripheral blood mononuclear cells by the mannoprotein of Cryptococcus neoformans involves human mannose binding protein.
3	9300722	We have shown previously that specific receptors on PBMCs and a serum factor other than Ab and complement are involved in the TNF-alpha response to cryptococcal mannoprotein (MP2).
4	9300722	Beta-Glucan laminarin produced background inhibition. mAbs against CD14, CD11b, and CD18 did not prevent FITC-MP2 binding to PBMCs, implying that these receptors are not involved in MP2 recognition by PBMCs. mAb against CD14 blocked (>90%) MP2-induced TNF-alpha release by PBMCs, while mAbs against CD11b/CD18 caused no inhibition.
5	9300722	Removal of human mannose binding protein (hMBP) by preincubation of serum with a specific mAb abrogated TNF-alpha induction by MP2 and strongly inhibited its binding to PBMCs.
6	9300722	Recombinant hMBP enhanced TNF-alpha induction by MP2 as well as binding of FITC-MP2 to PBMCs.
7	9300722	In addition, incubation of serum with MP2-coated beads and analysis by SDS-PAGE resulted in the detection of a protein of approximately 33/34 kDa that could be partially removed by preincubating the serum with hMBP mAb.
8	9300722	We conclude that hMBP is involved in the binding of MP2 to PBMCs and the release of TNF-alpha.
9	9300722	Induction of TNF-alpha in human peripheral blood mononuclear cells by the mannoprotein of Cryptococcus neoformans involves human mannose binding protein.
10	9300722	We have shown previously that specific receptors on PBMCs and a serum factor other than Ab and complement are involved in the TNF-alpha response to cryptococcal mannoprotein (MP2).
11	9300722	Beta-Glucan laminarin produced background inhibition. mAbs against CD14, CD11b, and CD18 did not prevent FITC-MP2 binding to PBMCs, implying that these receptors are not involved in MP2 recognition by PBMCs. mAb against CD14 blocked (>90%) MP2-induced TNF-alpha release by PBMCs, while mAbs against CD11b/CD18 caused no inhibition.
12	9300722	Removal of human mannose binding protein (hMBP) by preincubation of serum with a specific mAb abrogated TNF-alpha induction by MP2 and strongly inhibited its binding to PBMCs.
13	9300722	Recombinant hMBP enhanced TNF-alpha induction by MP2 as well as binding of FITC-MP2 to PBMCs.
14	9300722	In addition, incubation of serum with MP2-coated beads and analysis by SDS-PAGE resulted in the detection of a protein of approximately 33/34 kDa that could be partially removed by preincubating the serum with hMBP mAb.
15	9300722	We conclude that hMBP is involved in the binding of MP2 to PBMCs and the release of TNF-alpha.
16	9300722	Induction of TNF-alpha in human peripheral blood mononuclear cells by the mannoprotein of Cryptococcus neoformans involves human mannose binding protein.
17	9300722	We have shown previously that specific receptors on PBMCs and a serum factor other than Ab and complement are involved in the TNF-alpha response to cryptococcal mannoprotein (MP2).
18	9300722	Beta-Glucan laminarin produced background inhibition. mAbs against CD14, CD11b, and CD18 did not prevent FITC-MP2 binding to PBMCs, implying that these receptors are not involved in MP2 recognition by PBMCs. mAb against CD14 blocked (>90%) MP2-induced TNF-alpha release by PBMCs, while mAbs against CD11b/CD18 caused no inhibition.
19	9300722	Removal of human mannose binding protein (hMBP) by preincubation of serum with a specific mAb abrogated TNF-alpha induction by MP2 and strongly inhibited its binding to PBMCs.
20	9300722	Recombinant hMBP enhanced TNF-alpha induction by MP2 as well as binding of FITC-MP2 to PBMCs.
21	9300722	In addition, incubation of serum with MP2-coated beads and analysis by SDS-PAGE resulted in the detection of a protein of approximately 33/34 kDa that could be partially removed by preincubating the serum with hMBP mAb.
22	9300722	We conclude that hMBP is involved in the binding of MP2 to PBMCs and the release of TNF-alpha.
23	9300722	Induction of TNF-alpha in human peripheral blood mononuclear cells by the mannoprotein of Cryptococcus neoformans involves human mannose binding protein.
24	9300722	We have shown previously that specific receptors on PBMCs and a serum factor other than Ab and complement are involved in the TNF-alpha response to cryptococcal mannoprotein (MP2).
25	9300722	Beta-Glucan laminarin produced background inhibition. mAbs against CD14, CD11b, and CD18 did not prevent FITC-MP2 binding to PBMCs, implying that these receptors are not involved in MP2 recognition by PBMCs. mAb against CD14 blocked (>90%) MP2-induced TNF-alpha release by PBMCs, while mAbs against CD11b/CD18 caused no inhibition.
26	9300722	Removal of human mannose binding protein (hMBP) by preincubation of serum with a specific mAb abrogated TNF-alpha induction by MP2 and strongly inhibited its binding to PBMCs.
27	9300722	Recombinant hMBP enhanced TNF-alpha induction by MP2 as well as binding of FITC-MP2 to PBMCs.
28	9300722	In addition, incubation of serum with MP2-coated beads and analysis by SDS-PAGE resulted in the detection of a protein of approximately 33/34 kDa that could be partially removed by preincubating the serum with hMBP mAb.
29	9300722	We conclude that hMBP is involved in the binding of MP2 to PBMCs and the release of TNF-alpha.
30	9300722	Induction of TNF-alpha in human peripheral blood mononuclear cells by the mannoprotein of Cryptococcus neoformans involves human mannose binding protein.
31	9300722	We have shown previously that specific receptors on PBMCs and a serum factor other than Ab and complement are involved in the TNF-alpha response to cryptococcal mannoprotein (MP2).
32	9300722	Beta-Glucan laminarin produced background inhibition. mAbs against CD14, CD11b, and CD18 did not prevent FITC-MP2 binding to PBMCs, implying that these receptors are not involved in MP2 recognition by PBMCs. mAb against CD14 blocked (>90%) MP2-induced TNF-alpha release by PBMCs, while mAbs against CD11b/CD18 caused no inhibition.
33	9300722	Removal of human mannose binding protein (hMBP) by preincubation of serum with a specific mAb abrogated TNF-alpha induction by MP2 and strongly inhibited its binding to PBMCs.
34	9300722	Recombinant hMBP enhanced TNF-alpha induction by MP2 as well as binding of FITC-MP2 to PBMCs.
35	9300722	In addition, incubation of serum with MP2-coated beads and analysis by SDS-PAGE resulted in the detection of a protein of approximately 33/34 kDa that could be partially removed by preincubating the serum with hMBP mAb.
36	9300722	We conclude that hMBP is involved in the binding of MP2 to PBMCs and the release of TNF-alpha.
37	12455868	In this study we determined the levels of known humoral mediators of mycobacterial phagocytosis, i.e. mannose-binding lectin (MBL), soluble CD14 (sCD14), antibodies of the immunoglobulin G (IgG) class against mycobacterial purified protein derivative (PPD), and mycobacterial Hsp65 antigen, in the sera from healthy young volunteers vaccinated with BCG and presenting positive and negative Mantoux responses to PPD.
38	16099048	We identified A/B individuals as a unique group with large variation in MBL level, mannan binding activity and C4 deposition and propose a model for C4 deposition based on differential binding of MASP.
39	17983270	Gp120 from the HIV-1 strain JR-FL induced IL-10 expression in MDDCs from 62% of donors, via a mannose C-type lectin receptor(s) (MCLR).
40	17983270	The mannose-binding protein cyanovirin-N, the 2G12 mAb to a mannose-dependent gp120 epitope, and MCLR-specific mAbs inhibited IL-10 expression, as did enzymatic removal of gp120 mannose moieties, whereas inhibitors of signaling via CD4, CCR5, or CXCR4 were ineffective.
41	17983270	Gp120-stimulated IL-10 production correlated with DC-SIGN expression on the cells, and involved the ERK signaling pathway.
42	18288962	However, in the absence of danger, such as during the clearance of apoptotic cells, defense collagens such as C1q, MBL, ficolins, SP-A, SP-D and even adiponectin have all been shown to facilitate enhanced phagocytosis and modulate induction of cytokines towards an anti-inflammatory profile.
43	18996748	MBL interacts with IgM, resulting in the activation of MBL-associated serine proteases (MASPs), thus is initiating a lectin complement pathway.
44	19388159	The importance of complement recognition molecules (MBL, ficolins, factor H, C3, C1q, properdin, and others) to human disease are becoming clear as analysis of genetic data and knock out animals reveals links between complement proteins and specific diseases.
45	20042521	Gene polymorphisms, giving rise to low serum levels of mannose-binding lectin (MBL) or MBL-associated protease 2 (MASP2), have been associated with an increased risk of infections.
46	20042521	The objective of this study was to assess the outcome of intensive care unit (ICU) patients with systemic inflammatory response syndrome (SIRS) regarding the existence of functionally relevant MBL2 and MASP2 gene polymorphisms.
47	20042521	MBL2 and MASP2 single nucleotide polymorphisms were genotyped using a sequence-based typing technique.
48	20042521	Gene polymorphisms, giving rise to low serum levels of mannose-binding lectin (MBL) or MBL-associated protease 2 (MASP2), have been associated with an increased risk of infections.
49	20042521	The objective of this study was to assess the outcome of intensive care unit (ICU) patients with systemic inflammatory response syndrome (SIRS) regarding the existence of functionally relevant MBL2 and MASP2 gene polymorphisms.
50	20042521	MBL2 and MASP2 single nucleotide polymorphisms were genotyped using a sequence-based typing technique.
51	20042521	Gene polymorphisms, giving rise to low serum levels of mannose-binding lectin (MBL) or MBL-associated protease 2 (MASP2), have been associated with an increased risk of infections.
52	20042521	The objective of this study was to assess the outcome of intensive care unit (ICU) patients with systemic inflammatory response syndrome (SIRS) regarding the existence of functionally relevant MBL2 and MASP2 gene polymorphisms.
53	20042521	MBL2 and MASP2 single nucleotide polymorphisms were genotyped using a sequence-based typing technique.
54	20150204	We aimed to determine the association between invasive pneumococcal disease and MBL2 and MASP2 genetic variants, regarding serotype distribution.
55	20150204	Sequence-based typing analysis of amplicons covering the polymorphic regions of MASP2 (exon 3) and MBL2 (promoter and exon 1) was performed.
56	20150204	We aimed to determine the association between invasive pneumococcal disease and MBL2 and MASP2 genetic variants, regarding serotype distribution.
57	20150204	Sequence-based typing analysis of amplicons covering the polymorphic regions of MASP2 (exon 3) and MBL2 (promoter and exon 1) was performed.
58	23467824	By screening a series of peptides derived from the BTV16 VP2 protein and expressed as mannose-binding protein fusions, we determined that the linear epitopes recognized by the VP2-specific MAbs 3 G10 and 2B4 were located within the peptides 34EWSGHDVTEIPNRRMF49 and 540KNEDPYVKRTVKPIRA555, respectively.
59	23467824	To define the minimal region required for antibody binding within these peptide regions, a series of progressively shorter peptides were synthesized and evaluated for 3 G10 and 2B4 binding.
60	23467824	This work defined the motifs 34EWSGHDVTEIPNRRMF49 and 543DPYVKRTVK555 as the minimal linear peptides required for 3 G10 and 2B4 binding, respectively.
61	23595505	Genetic variants in toll-like receptor 2 (TLR2), TLR4, TLR9, and FCγ receptor II are associated with antibody response to quadrivalent meningococcal conjugate vaccine in HIV-infected youth.
62	23595505	Genetic variants associated with severity of meningococcal disease, including the IgG Fc receptor (FCγRII)-A484T, interleukin-10 (IL-10)-A1082G, -C819T, and -C627A, IL-4-C589T, mannose binding lectin-2 (MBL2)-A/O, -H/L, -P/Q, and -X/Y, toll-like receptor 2 (TLR2)-G2408A, TLR4-A12874G and -C13174T, and TLR9-T1237C and -T1486C were determined by real-time PCR (RT-PCR) for 271 HIV-infected subjects (median, 17 years).
63	23595505	These findings suggest that for HIV-infected youth, the initial antibody response to MCV4 is associated with variants in TLR2 and TLR4 while the long-term response is associated with genetic polymorphisms in TLR9 and FcγRIIa.
64	24173025	Blood collection tubes influence serum ficolin-1 and ficolin-2 levels.
65	24173025	Ficolin-1 (M-ficolin) and ficolin-2 (L-ficolin) are known to bind Streptococcus pneumoniae serotypes 19C and 11A, respectively.
66	24173025	We found that the silica clot activator eluted from plastic red-top tubes inhibited ficolin-2 ligand binding, while other related proteins, like mannose-binding lectin (MBL) and ficolin-1, were not affected.
67	24173025	These tube types did not affect the concentrations of other related opsonins (C1q, MBL, or ficolin-3 [H-ficolin]).
68	24173025	These findings have implications for future ficolin-1 and ficolin-2 studies, as proper sample collection and handling are essential.
69	24173025	Blood collection tubes influence serum ficolin-1 and ficolin-2 levels.
70	24173025	Ficolin-1 (M-ficolin) and ficolin-2 (L-ficolin) are known to bind Streptococcus pneumoniae serotypes 19C and 11A, respectively.
71	24173025	We found that the silica clot activator eluted from plastic red-top tubes inhibited ficolin-2 ligand binding, while other related proteins, like mannose-binding lectin (MBL) and ficolin-1, were not affected.
72	24173025	These tube types did not affect the concentrations of other related opsonins (C1q, MBL, or ficolin-3 [H-ficolin]).
73	24173025	These findings have implications for future ficolin-1 and ficolin-2 studies, as proper sample collection and handling are essential.
74	25030054	The ficolins are a family of innate pattern recognition molecules that are known to bind acetylated compounds and activate complement through the association of mannose binding lectin (MBL)/ficolin-associated serine proteases (MASPs).
75	25030054	While studying ficolin-2-mediated complement deposition on Streptococcus pneumoniae, we found that sera depleted of C1q or other complement components were also codepleted of ficolin-2 but not ficolin-1, ficolin-3, or MBL.
76	25030054	MBL present in C1q-depleted sera was able to mediate complement deposition on Saccharomyces cerevisiae, suggesting the presence of MASPs.
77	25030054	The ficolins are a family of innate pattern recognition molecules that are known to bind acetylated compounds and activate complement through the association of mannose binding lectin (MBL)/ficolin-associated serine proteases (MASPs).
78	25030054	While studying ficolin-2-mediated complement deposition on Streptococcus pneumoniae, we found that sera depleted of C1q or other complement components were also codepleted of ficolin-2 but not ficolin-1, ficolin-3, or MBL.
79	25030054	MBL present in C1q-depleted sera was able to mediate complement deposition on Saccharomyces cerevisiae, suggesting the presence of MASPs.
80	25030054	The ficolins are a family of innate pattern recognition molecules that are known to bind acetylated compounds and activate complement through the association of mannose binding lectin (MBL)/ficolin-associated serine proteases (MASPs).
81	25030054	While studying ficolin-2-mediated complement deposition on Streptococcus pneumoniae, we found that sera depleted of C1q or other complement components were also codepleted of ficolin-2 but not ficolin-1, ficolin-3, or MBL.
82	25030054	MBL present in C1q-depleted sera was able to mediate complement deposition on Saccharomyces cerevisiae, suggesting the presence of MASPs.
83	25649508	Increased expression of MBL, CRP, IFN-α, IL-1β, IL-8, IL-12β and IL-18 followed at week 6 p.i. and at both week 6 and 9 p.i. expression of DEFβ1 was highly increased in infected chickens.