Ignet

Gene Information

Gene symbol: CFH

Gene name: complement factor H

HGNC ID: 4883

Synonyms: HUS, FHL1, ARMS1

Related Genes

#	Gene Symbol	Number of hits
1	ADAMTS1	1 hits
2	C4B	1 hits
3	C4BPA	1 hits
4	C5AR1	1 hits
5	CAMP	1 hits
6	CD4	1 hits
7	CD46	1 hits
8	CD55	1 hits
9	CD79A	1 hits
10	CD8A	1 hits
11	CDKN1A	1 hits
12	CFHR1	1 hits
13	CFHR3	1 hits
14	CR1	1 hits
15	CR2	1 hits
16	EGF	1 hits
17	ELK3	1 hits
18	EPO	1 hits
19	FGF7	1 hits
20	GBA	1 hits
21	HGF	1 hits
22	MAGEA6	1 hits
23	MBL2	1 hits
24	PTPN11	1 hits
25	TF	1 hits
26	VDAC1	1 hits
27	VEGFA	1 hits
28	VTN	1 hits

Related Sentences

#	PMID	Sentence
1	9143703	DAF/CD55) or are secondarily attached to HIV envelope glycoproteins as in the case of factor H.
2	10885988	The strong resistance of the group A streptococcus to phagocytosis is related to factor H and fibrinogen binding by M protein and to disarming complement component C5a by the C5a peptidase.
3	12804166	Borrelial complement regulator acquiring proteins, among them OspE or Erp proteins, bind to host factor H and related proteins, and this binding protects against activation of complement by the spirochetal surface.
4	12914816	Several strains of all three species express molecules (M-proteins, Bac or beta, PspC) that acquire host fluid-phase complement regulators factor H or C4b binding protein to their surfaces.
5	15128807	Deleting 15-aa residues (region V) from the C terminus of the OspE paralog P21 (a 20.7-kDa OspE-paralogous surface lipoprotein in the B. burgdorferi sensu stricto 297 strain) abolished factor H binding.
6	15128807	However, C-terminal peptides from OspE, P21, or OspEF-related protein P alone and the C-terminal deletion mutants of P21 inhibited factor H binding to OspE only partially when compared with full-length P21 or its N-terminal mutant.
7	15128807	Deleting 15-aa residues (region V) from the C terminus of the OspE paralog P21 (a 20.7-kDa OspE-paralogous surface lipoprotein in the B. burgdorferi sensu stricto 297 strain) abolished factor H binding.
8	15128807	However, C-terminal peptides from OspE, P21, or OspEF-related protein P alone and the C-terminal deletion mutants of P21 inhibited factor H binding to OspE only partially when compared with full-length P21 or its N-terminal mutant.
9	16023794	The human complement RCA proteins analyzed were factor H (FH), C4 binding protein alpha chain, membrane cofactor protein (MCP), decay accelerating factor (DAF), and complement receptors type 1 (CR1) and 2 (CR2).
10	16023794	Sequences of key poxvirus regulators of complement activation, vaccinia virus complement control protein (VCP), smallpox inhibitor of complement enzymes (SPICE), and cowpox inflammation modulatory protein (IMP) were similar to SCRs 1 through 5 of C4 binding protein, alpha chain, and they were also clustered with other homologous repeats of MCP, DAF, CR1, CR2, and FH.
11	19264772	Additionally, JEV NS1 failed to bind complement factor H, in contrast to NS1 of West Nile virus, suggesting that the NS1 proteins of different flaviviruses have distinctly different mechanisms for interacting with the host.
12	19388158	Homozygous chromosomal deletion of a genomic 84 kb, chromosomal fragment which includes the genes CFHR1/CFHR3 is a risk factor for hemolytic uremic syndrome (HUS) at young age and is predominantly associated with the generation of autoantibodies to CFH, leading to a specific type of HUS, called DEAP (deficiency of CFHR and autoantibody positive)-HUS.
13	19388158	Thus CFHR1 and CFHR3 proteins, and likely also the other members of this gene family are linked to human diseases.
14	19388158	We here summarize the current knowledge about the role or association of CFHR1 and CFHR3 in the human diseases HUS and AMD.
15	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.
16	19388167	N. gonorrhoeae uses its outer membrane porin (Por) molecules to bind complement down-regulatory proteins, C4b-binding protein (C4BP) and factor H (fH), to evade killing by human complement.
17	19388169	Binding of the complement regulatory proteins factor H, factor H-like protein 1 (FHL-1), C4b-binding protein (C4BP), or CD46 is a crucial step in the pathogenesis of these infections.
18	19477524	However, a wide variety of bacterial pathogens subvert complement attack by binding host complement inhibitors such as C4b-binding protein, factor H and vitronectin, which results in diminished opsonophagocytosis and killing of bacteria by lysis.
19	19948796	Factor H binding protein (fHBP) is a surface-exposed lipoprotein in Neisseria meningitidis, which is a component of several investigational vaccines against serogroup B meningococcus (MenB) currently in development. fHBP enables the bacterium to evade complement-mediated killing by binding factor H, a key downregulator of the complement alternative pathway, and, in addition, fHBP is important for meningococcal survival in the presence of the antimicrobial peptide LL-37.
20	21402895	C4b deposition mediated by an anti-factor H-binding protein mAb was reduced by intact blocking IgG, but not by peptide:N-glycanase-treated blocking IgG, suggesting that blocking resulted from inhibition of classical pathway of complement.
21	21965688	The NHBA domain fold consists of an 8-strand β-barrel that closely resembles the C-terminal domains of N. meningitidis factor H-binding protein and transferrin-binding protein B.
22	22368277	Immune Abs against N. gonorrhoeae need to overcome several subversive mechanisms whereby gonococcus evades complement, including binding to C4b-binding protein (C4BP; classical pathway inhibitor) and factor H (alternative pathway [AP] inhibitor).
23	23485926	Complement components C3, C5, properdin and factor H were retained following the process and the IgG-depleted complement was shown to be suitable for use in antibody-mediated complement deposition and serum bactericidal activity assays against serogroup B meningococci.
24	24631075	Surface-expressed protein antigens such as factor H-binding protein (fHbp), Neisserial adhesin A (NadA), Neisserial heparin-binding antigen (NHBA) and Porin protein A (PorA); all express sequence variability that can affect their function as protective immunogens when used in meningococcal serogroup B vaccines like the recently-approved 4CMenB (Bexsero(®)).
25	25707694	Levels of IgG, IgM, and IgA, factor B, and factor H, polymorphisms of MBL and Fc-gamma receptors were determined.
26	25941307	We present a child with a hybrid CFH/CFHR3 gene who, having had multiple disease relapses despite optimal treatment with plasma exchange, commenced eculizumab therapy in August 2010.
27	25960935	Molecular mimicry of MAGE-A6 and Mycoplasma penetrans HF-2 epitopes in the induction of antitumor CD8⁺ T-cell responses.
28	25960935	A promising vaccine strategy for the treatment of cancer involves the use of vaccines incorporating tumor antigen-derived synthetic peptides that can be coordinately recognized by specific CD4⁺ and CD8⁺ T-cells.
29	25960935	Previously, we reported that a MAGE-A6-derived peptide (MAGE-A6_172-187) and its highly-immunogenic and cross-reactive homolog derived from Mycoplasma penetrans HF-2 permease (HF-2_216-229) are promiscuously presented by multiple HLA-DR alleles to responder CD4⁺ T-cells obtained from healthy donors and melanoma patients.
30	25960935	Here, we investigated whether these same peptides could concomitantly stimulate cross-reactive MAGE-A6-specific CD8⁺ T-cell responses in vitro using cells isolated from HLA-A*0201 (HLA-A2)⁺ healthy individuals and patients with melanoma.
31	25960935	We now show that MAGE-A6_172-187 and, even more so, HF-2_216-229, induce memory CD8⁺ T cells that recognize HLA-A2⁺ MAGE-A6⁺ tumor target cells.
32	25960935	The immunogenicity of these peptides was at least partially attributed to their embedded MAGE-A6_176-185 and HF-2_220-229 "homologous" sequences.
33	25960935	The functional avidity of HF-2_216-229 peptide-primed CD8⁺ T cells for the MAGE-A6_172-187 peptide was more than 100-fold greater than that of CD8⁺ T cells primed with the corresponding MAGE-A6 peptide.
34	25960935	Additionally, these 2 peptides were recognized in interferon γ (IFNγ) and granzyme B ELISPOT assays by CD8⁺ T-cell clones displaying variable T-cell receptor (TCR) Vβ usage.
35	25960935	These data suggest that the immune cross-reactivity of the MAGE-A6_172-187 and HF-2_216-229 peptides extends to CD8⁺ T cells, at least in HLA-A2⁺ donors, and supports the potential translational utility of these epitopes in clinical vaccine formulations and for immunomonitoring of cancer patients.
36	25960935	Molecular mimicry of MAGE-A6 and Mycoplasma penetrans HF-2 epitopes in the induction of antitumor CD8⁺ T-cell responses.
37	25960935	A promising vaccine strategy for the treatment of cancer involves the use of vaccines incorporating tumor antigen-derived synthetic peptides that can be coordinately recognized by specific CD4⁺ and CD8⁺ T-cells.
38	25960935	Previously, we reported that a MAGE-A6-derived peptide (MAGE-A6_172-187) and its highly-immunogenic and cross-reactive homolog derived from Mycoplasma penetrans HF-2 permease (HF-2_216-229) are promiscuously presented by multiple HLA-DR alleles to responder CD4⁺ T-cells obtained from healthy donors and melanoma patients.
39	25960935	Here, we investigated whether these same peptides could concomitantly stimulate cross-reactive MAGE-A6-specific CD8⁺ T-cell responses in vitro using cells isolated from HLA-A*0201 (HLA-A2)⁺ healthy individuals and patients with melanoma.
40	25960935	We now show that MAGE-A6_172-187 and, even more so, HF-2_216-229, induce memory CD8⁺ T cells that recognize HLA-A2⁺ MAGE-A6⁺ tumor target cells.
41	25960935	The immunogenicity of these peptides was at least partially attributed to their embedded MAGE-A6_176-185 and HF-2_220-229 "homologous" sequences.
42	25960935	The functional avidity of HF-2_216-229 peptide-primed CD8⁺ T cells for the MAGE-A6_172-187 peptide was more than 100-fold greater than that of CD8⁺ T cells primed with the corresponding MAGE-A6 peptide.
43	25960935	Additionally, these 2 peptides were recognized in interferon γ (IFNγ) and granzyme B ELISPOT assays by CD8⁺ T-cell clones displaying variable T-cell receptor (TCR) Vβ usage.
44	25960935	These data suggest that the immune cross-reactivity of the MAGE-A6_172-187 and HF-2_216-229 peptides extends to CD8⁺ T cells, at least in HLA-A2⁺ donors, and supports the potential translational utility of these epitopes in clinical vaccine formulations and for immunomonitoring of cancer patients.
45	25960935	Molecular mimicry of MAGE-A6 and Mycoplasma penetrans HF-2 epitopes in the induction of antitumor CD8⁺ T-cell responses.
46	25960935	A promising vaccine strategy for the treatment of cancer involves the use of vaccines incorporating tumor antigen-derived synthetic peptides that can be coordinately recognized by specific CD4⁺ and CD8⁺ T-cells.
47	25960935	Previously, we reported that a MAGE-A6-derived peptide (MAGE-A6_172-187) and its highly-immunogenic and cross-reactive homolog derived from Mycoplasma penetrans HF-2 permease (HF-2_216-229) are promiscuously presented by multiple HLA-DR alleles to responder CD4⁺ T-cells obtained from healthy donors and melanoma patients.
48	25960935	Here, we investigated whether these same peptides could concomitantly stimulate cross-reactive MAGE-A6-specific CD8⁺ T-cell responses in vitro using cells isolated from HLA-A*0201 (HLA-A2)⁺ healthy individuals and patients with melanoma.
49	25960935	We now show that MAGE-A6_172-187 and, even more so, HF-2_216-229, induce memory CD8⁺ T cells that recognize HLA-A2⁺ MAGE-A6⁺ tumor target cells.
50	25960935	The immunogenicity of these peptides was at least partially attributed to their embedded MAGE-A6_176-185 and HF-2_220-229 "homologous" sequences.
51	25960935	The functional avidity of HF-2_216-229 peptide-primed CD8⁺ T cells for the MAGE-A6_172-187 peptide was more than 100-fold greater than that of CD8⁺ T cells primed with the corresponding MAGE-A6 peptide.
52	25960935	Additionally, these 2 peptides were recognized in interferon γ (IFNγ) and granzyme B ELISPOT assays by CD8⁺ T-cell clones displaying variable T-cell receptor (TCR) Vβ usage.
53	25960935	These data suggest that the immune cross-reactivity of the MAGE-A6_172-187 and HF-2_216-229 peptides extends to CD8⁺ T cells, at least in HLA-A2⁺ donors, and supports the potential translational utility of these epitopes in clinical vaccine formulations and for immunomonitoring of cancer patients.
54	25960935	Molecular mimicry of MAGE-A6 and Mycoplasma penetrans HF-2 epitopes in the induction of antitumor CD8⁺ T-cell responses.
55	25960935	A promising vaccine strategy for the treatment of cancer involves the use of vaccines incorporating tumor antigen-derived synthetic peptides that can be coordinately recognized by specific CD4⁺ and CD8⁺ T-cells.
56	25960935	Previously, we reported that a MAGE-A6-derived peptide (MAGE-A6_172-187) and its highly-immunogenic and cross-reactive homolog derived from Mycoplasma penetrans HF-2 permease (HF-2_216-229) are promiscuously presented by multiple HLA-DR alleles to responder CD4⁺ T-cells obtained from healthy donors and melanoma patients.
57	25960935	Here, we investigated whether these same peptides could concomitantly stimulate cross-reactive MAGE-A6-specific CD8⁺ T-cell responses in vitro using cells isolated from HLA-A*0201 (HLA-A2)⁺ healthy individuals and patients with melanoma.
58	25960935	We now show that MAGE-A6_172-187 and, even more so, HF-2_216-229, induce memory CD8⁺ T cells that recognize HLA-A2⁺ MAGE-A6⁺ tumor target cells.
59	25960935	The immunogenicity of these peptides was at least partially attributed to their embedded MAGE-A6_176-185 and HF-2_220-229 "homologous" sequences.
60	25960935	The functional avidity of HF-2_216-229 peptide-primed CD8⁺ T cells for the MAGE-A6_172-187 peptide was more than 100-fold greater than that of CD8⁺ T cells primed with the corresponding MAGE-A6 peptide.
61	25960935	Additionally, these 2 peptides were recognized in interferon γ (IFNγ) and granzyme B ELISPOT assays by CD8⁺ T-cell clones displaying variable T-cell receptor (TCR) Vβ usage.
62	25960935	These data suggest that the immune cross-reactivity of the MAGE-A6_172-187 and HF-2_216-229 peptides extends to CD8⁺ T cells, at least in HLA-A2⁺ donors, and supports the potential translational utility of these epitopes in clinical vaccine formulations and for immunomonitoring of cancer patients.
63	25960935	Molecular mimicry of MAGE-A6 and Mycoplasma penetrans HF-2 epitopes in the induction of antitumor CD8⁺ T-cell responses.
64	25960935	A promising vaccine strategy for the treatment of cancer involves the use of vaccines incorporating tumor antigen-derived synthetic peptides that can be coordinately recognized by specific CD4⁺ and CD8⁺ T-cells.
65	25960935	Previously, we reported that a MAGE-A6-derived peptide (MAGE-A6_172-187) and its highly-immunogenic and cross-reactive homolog derived from Mycoplasma penetrans HF-2 permease (HF-2_216-229) are promiscuously presented by multiple HLA-DR alleles to responder CD4⁺ T-cells obtained from healthy donors and melanoma patients.
66	25960935	Here, we investigated whether these same peptides could concomitantly stimulate cross-reactive MAGE-A6-specific CD8⁺ T-cell responses in vitro using cells isolated from HLA-A*0201 (HLA-A2)⁺ healthy individuals and patients with melanoma.
67	25960935	We now show that MAGE-A6_172-187 and, even more so, HF-2_216-229, induce memory CD8⁺ T cells that recognize HLA-A2⁺ MAGE-A6⁺ tumor target cells.
68	25960935	The immunogenicity of these peptides was at least partially attributed to their embedded MAGE-A6_176-185 and HF-2_220-229 "homologous" sequences.
69	25960935	The functional avidity of HF-2_216-229 peptide-primed CD8⁺ T cells for the MAGE-A6_172-187 peptide was more than 100-fold greater than that of CD8⁺ T cells primed with the corresponding MAGE-A6 peptide.
70	25960935	Additionally, these 2 peptides were recognized in interferon γ (IFNγ) and granzyme B ELISPOT assays by CD8⁺ T-cell clones displaying variable T-cell receptor (TCR) Vβ usage.
71	25960935	These data suggest that the immune cross-reactivity of the MAGE-A6_172-187 and HF-2_216-229 peptides extends to CD8⁺ T cells, at least in HLA-A2⁺ donors, and supports the potential translational utility of these epitopes in clinical vaccine formulations and for immunomonitoring of cancer patients.
72	25960935	Molecular mimicry of MAGE-A6 and Mycoplasma penetrans HF-2 epitopes in the induction of antitumor CD8⁺ T-cell responses.
73	25960935	A promising vaccine strategy for the treatment of cancer involves the use of vaccines incorporating tumor antigen-derived synthetic peptides that can be coordinately recognized by specific CD4⁺ and CD8⁺ T-cells.
74	25960935	Previously, we reported that a MAGE-A6-derived peptide (MAGE-A6_172-187) and its highly-immunogenic and cross-reactive homolog derived from Mycoplasma penetrans HF-2 permease (HF-2_216-229) are promiscuously presented by multiple HLA-DR alleles to responder CD4⁺ T-cells obtained from healthy donors and melanoma patients.
75	25960935	Here, we investigated whether these same peptides could concomitantly stimulate cross-reactive MAGE-A6-specific CD8⁺ T-cell responses in vitro using cells isolated from HLA-A*0201 (HLA-A2)⁺ healthy individuals and patients with melanoma.
76	25960935	We now show that MAGE-A6_172-187 and, even more so, HF-2_216-229, induce memory CD8⁺ T cells that recognize HLA-A2⁺ MAGE-A6⁺ tumor target cells.
77	25960935	The immunogenicity of these peptides was at least partially attributed to their embedded MAGE-A6_176-185 and HF-2_220-229 "homologous" sequences.
78	25960935	The functional avidity of HF-2_216-229 peptide-primed CD8⁺ T cells for the MAGE-A6_172-187 peptide was more than 100-fold greater than that of CD8⁺ T cells primed with the corresponding MAGE-A6 peptide.
79	25960935	Additionally, these 2 peptides were recognized in interferon γ (IFNγ) and granzyme B ELISPOT assays by CD8⁺ T-cell clones displaying variable T-cell receptor (TCR) Vβ usage.
80	25960935	These data suggest that the immune cross-reactivity of the MAGE-A6_172-187 and HF-2_216-229 peptides extends to CD8⁺ T cells, at least in HLA-A2⁺ donors, and supports the potential translational utility of these epitopes in clinical vaccine formulations and for immunomonitoring of cancer patients.
81	26011014	Among the products are tumour-directed monoclonal antibodies with enhanced antibody-dependent cytotoxicity (ADCC), vascular endothelial growth factor (VEGF), complement factor H (FH), keratinocyte growth factor (FGF7/KGF), epidermal growth factor (EGF), hepatocyte growth factor (HGF), asialo-erythropoietin (asialo-EPO, AEPO), alpha-galactosidase (aGal) and beta-glucocerebrosidase (GBA).
82	26200783	Several strains of GAS bind to human-specific complement inhibitors, C4b-binding protein (C4BP) and/or Factor H (FH), to curtail complement C3 (a critical opsonin) deposition.
83	26368279	Interaction with the complement components C1q, C3b, C4BP, and factor H was explored whereas opsonophagocytosis assays were performed using a human cell line differentiated to neutrophils.
84	26457721	To inactivate C3b, the parasites bind FH as well as related proteins FHL-1 and CFHR-1 to their surface, and FH binding is trypsin-resistant.