Ignet

Gene Information

Gene symbol: CR1

Gene name: complement component (3b/4b) receptor 1 (Knops blood group)

HGNC ID: 2334

Synonyms: CD35, KN

Related Genes

#	Gene Symbol	Number of hits
1	C4B	1 hits
2	C5AR1	1 hits
3	CCR2	1 hits
4	CD209	1 hits
5	CD4	1 hits
6	CD83	1 hits
7	CD86	1 hits
8	CD8A	1 hits
9	CR2	1 hits
10	IDDM2	1 hits
11	IFNG	1 hits
12	IL1B	1 hits
13	IL2	1 hits
14	INS	1 hits
15	ITGAM	1 hits
16	SELL	1 hits
17	TDGF3	1 hits

Related Sentences

#	PMID	Sentence
1	1352745	Normal C3b receptor (CR1) genomic polymorphism in patients with insulin-dependent diabetes mellitus (IDDM): is the low erythrocyte CR1 expression an acquired phenomenon?
2	1352745	Expression of the erythrocyte complement receptor (C3bR = CR1 = CD35) and its genomic polymorphism (HindIII RFLP) was studied in a group of 80 patients with IDDM, 31 healthy siblings and 101 healthy blood donors.
3	1352745	Defective CR1 expression was found in 26% of the patients with IDDM compared with 9% of the controls (P less than 0.05) and 0% of the siblings.
4	1352745	The CR1 gene polymorphism of the IDDM patients did not significantly differ from that of the controls.
5	1352745	No significant association was found between the presence or absence of the HLA risk antigens for IDDM and CR1 expression.
6	1352745	The results confirm that erythrocyte CR1 expression is genetically determined, but the CR1 deficiency associated with IDDM seems to be an acquired rather than a genetic phenomenon.
7	1352745	Normal C3b receptor (CR1) genomic polymorphism in patients with insulin-dependent diabetes mellitus (IDDM): is the low erythrocyte CR1 expression an acquired phenomenon?
8	1352745	Expression of the erythrocyte complement receptor (C3bR = CR1 = CD35) and its genomic polymorphism (HindIII RFLP) was studied in a group of 80 patients with IDDM, 31 healthy siblings and 101 healthy blood donors.
9	1352745	Defective CR1 expression was found in 26% of the patients with IDDM compared with 9% of the controls (P less than 0.05) and 0% of the siblings.
10	1352745	The CR1 gene polymorphism of the IDDM patients did not significantly differ from that of the controls.
11	1352745	No significant association was found between the presence or absence of the HLA risk antigens for IDDM and CR1 expression.
12	1352745	The results confirm that erythrocyte CR1 expression is genetically determined, but the CR1 deficiency associated with IDDM seems to be an acquired rather than a genetic phenomenon.
13	1352745	Normal C3b receptor (CR1) genomic polymorphism in patients with insulin-dependent diabetes mellitus (IDDM): is the low erythrocyte CR1 expression an acquired phenomenon?
14	1352745	Expression of the erythrocyte complement receptor (C3bR = CR1 = CD35) and its genomic polymorphism (HindIII RFLP) was studied in a group of 80 patients with IDDM, 31 healthy siblings and 101 healthy blood donors.
15	1352745	Defective CR1 expression was found in 26% of the patients with IDDM compared with 9% of the controls (P less than 0.05) and 0% of the siblings.
16	1352745	The CR1 gene polymorphism of the IDDM patients did not significantly differ from that of the controls.
17	1352745	No significant association was found between the presence or absence of the HLA risk antigens for IDDM and CR1 expression.
18	1352745	The results confirm that erythrocyte CR1 expression is genetically determined, but the CR1 deficiency associated with IDDM seems to be an acquired rather than a genetic phenomenon.
19	1352745	Normal C3b receptor (CR1) genomic polymorphism in patients with insulin-dependent diabetes mellitus (IDDM): is the low erythrocyte CR1 expression an acquired phenomenon?
20	1352745	Expression of the erythrocyte complement receptor (C3bR = CR1 = CD35) and its genomic polymorphism (HindIII RFLP) was studied in a group of 80 patients with IDDM, 31 healthy siblings and 101 healthy blood donors.
21	1352745	Defective CR1 expression was found in 26% of the patients with IDDM compared with 9% of the controls (P less than 0.05) and 0% of the siblings.
22	1352745	The CR1 gene polymorphism of the IDDM patients did not significantly differ from that of the controls.
23	1352745	No significant association was found between the presence or absence of the HLA risk antigens for IDDM and CR1 expression.
24	1352745	The results confirm that erythrocyte CR1 expression is genetically determined, but the CR1 deficiency associated with IDDM seems to be an acquired rather than a genetic phenomenon.
25	1352745	Normal C3b receptor (CR1) genomic polymorphism in patients with insulin-dependent diabetes mellitus (IDDM): is the low erythrocyte CR1 expression an acquired phenomenon?
26	1352745	Expression of the erythrocyte complement receptor (C3bR = CR1 = CD35) and its genomic polymorphism (HindIII RFLP) was studied in a group of 80 patients with IDDM, 31 healthy siblings and 101 healthy blood donors.
27	1352745	Defective CR1 expression was found in 26% of the patients with IDDM compared with 9% of the controls (P less than 0.05) and 0% of the siblings.
28	1352745	The CR1 gene polymorphism of the IDDM patients did not significantly differ from that of the controls.
29	1352745	No significant association was found between the presence or absence of the HLA risk antigens for IDDM and CR1 expression.
30	1352745	The results confirm that erythrocyte CR1 expression is genetically determined, but the CR1 deficiency associated with IDDM seems to be an acquired rather than a genetic phenomenon.
31	1352745	Normal C3b receptor (CR1) genomic polymorphism in patients with insulin-dependent diabetes mellitus (IDDM): is the low erythrocyte CR1 expression an acquired phenomenon?
32	1352745	Expression of the erythrocyte complement receptor (C3bR = CR1 = CD35) and its genomic polymorphism (HindIII RFLP) was studied in a group of 80 patients with IDDM, 31 healthy siblings and 101 healthy blood donors.
33	1352745	Defective CR1 expression was found in 26% of the patients with IDDM compared with 9% of the controls (P less than 0.05) and 0% of the siblings.
34	1352745	The CR1 gene polymorphism of the IDDM patients did not significantly differ from that of the controls.
35	1352745	No significant association was found between the presence or absence of the HLA risk antigens for IDDM and CR1 expression.
36	1352745	The results confirm that erythrocyte CR1 expression is genetically determined, but the CR1 deficiency associated with IDDM seems to be an acquired rather than a genetic phenomenon.
37	6223755	The complement receptor for C3b of the epithelial cells of human glomeruli is structurally and functionally very similar or identical to CR1, the complement receptor for C3b and C4b present on the membrane of red cells and leukocytes.
38	6235073	Defective erythrocyte C3b receptor function associated with low serum complement (C3, C4) concentrations in insulin-dependent diabetes mellitus.
39	6235073	An immune adherence haemagglutination (IAHA) method was used to measure erythrocyte C3b receptor (EC3bR) activity in 110 patients with insulin-dependent diabetes mellitus (IDDM) and 223 controls.
40	6235073	Defective erythrocyte C3b receptor function associated with low serum complement (C3, C4) concentrations in insulin-dependent diabetes mellitus.
41	6235073	An immune adherence haemagglutination (IAHA) method was used to measure erythrocyte C3b receptor (EC3bR) activity in 110 patients with insulin-dependent diabetes mellitus (IDDM) and 223 controls.
42	7587921	This study was undertaken to determine whether this reduced lymphocyte proliferation is mediated by a decreased production of cytokine or decreased expression of interleukin-2 receptor (IL-2R).
43	7587921	However, the production of IL-1 beta, IL-2 and interferon-gamma, the percentages of pan T cells (CD3), T helper cells (CD4), T suppressor cells (CD8), the ratio of CD4/CD8 and the expression of CR1 and Fc receptors for immunoglobulin G (Fc gamma RII and Fc gamma RIII) were not significantly different between NIDDM patients and healthy subjects.
44	7587921	These findings suggest that decreased expression of CR3 on monocytes, decreased lymphocyte proliferation and decreased IL-2R expression despite a higher production of TNF-alpha may explain the impaired cell-mediated immunity seen in NIDDM patients.
45	8579484	One of the anaphylatoxins, C5a, possesses both the strong biological activity of a chemotactic factor and the increasing effect of CR1 and CR3 expression on polymorphonuclear leukocytes (PMNs).
46	8579484	It is well known that the complement receptors, CR1 and CR3, on PMNs play important roles in the phagocytosis.
47	8579484	We studied the changes of the expression of these receptors on PMNs in non-insulin dependent diabetes mellitus after the stimulation with recombinant human C5a.
48	8579484	There was no significant difference of CR1 and CR3 expression on PMNs after the addition of 10 ng/ml C5a between patients with diabetes mellitus and normal controls.
49	8579484	One of the anaphylatoxins, C5a, possesses both the strong biological activity of a chemotactic factor and the increasing effect of CR1 and CR3 expression on polymorphonuclear leukocytes (PMNs).
50	8579484	It is well known that the complement receptors, CR1 and CR3, on PMNs play important roles in the phagocytosis.
51	8579484	We studied the changes of the expression of these receptors on PMNs in non-insulin dependent diabetes mellitus after the stimulation with recombinant human C5a.
52	8579484	There was no significant difference of CR1 and CR3 expression on PMNs after the addition of 10 ng/ml C5a between patients with diabetes mellitus and normal controls.
53	8579484	One of the anaphylatoxins, C5a, possesses both the strong biological activity of a chemotactic factor and the increasing effect of CR1 and CR3 expression on polymorphonuclear leukocytes (PMNs).
54	8579484	It is well known that the complement receptors, CR1 and CR3, on PMNs play important roles in the phagocytosis.
55	8579484	We studied the changes of the expression of these receptors on PMNs in non-insulin dependent diabetes mellitus after the stimulation with recombinant human C5a.
56	8579484	There was no significant difference of CR1 and CR3 expression on PMNs after the addition of 10 ng/ml C5a between patients with diabetes mellitus and normal controls.
57	10433799	Contribution of the innate immune system to autoimmune diabetes: a role for the CR1/CR2 complement receptors.
58	10433799	The complement component of the innate immune system regulates B cell activation and tolerance through complement receptors CR1/CR2.
59	10433799	Examination of the lymphoid compartments of NOD mice revealed striking expansion of a splenic B cell subset with high cell surface expression of CR1/CR2.
60	10433799	Importantly, long-term in vivo blockade of C3 binding to CR1/CR2 prevented the emergence of the CR1/CR2(hi) B cells and afforded resistance to autoimmune diabetes in NOD mice.
61	10433799	Contribution of the innate immune system to autoimmune diabetes: a role for the CR1/CR2 complement receptors.
62	10433799	The complement component of the innate immune system regulates B cell activation and tolerance through complement receptors CR1/CR2.
63	10433799	Examination of the lymphoid compartments of NOD mice revealed striking expansion of a splenic B cell subset with high cell surface expression of CR1/CR2.
64	10433799	Importantly, long-term in vivo blockade of C3 binding to CR1/CR2 prevented the emergence of the CR1/CR2(hi) B cells and afforded resistance to autoimmune diabetes in NOD mice.
65	10433799	Contribution of the innate immune system to autoimmune diabetes: a role for the CR1/CR2 complement receptors.
66	10433799	The complement component of the innate immune system regulates B cell activation and tolerance through complement receptors CR1/CR2.
67	10433799	Examination of the lymphoid compartments of NOD mice revealed striking expansion of a splenic B cell subset with high cell surface expression of CR1/CR2.
68	10433799	Importantly, long-term in vivo blockade of C3 binding to CR1/CR2 prevented the emergence of the CR1/CR2(hi) B cells and afforded resistance to autoimmune diabetes in NOD mice.
69	10433799	Contribution of the innate immune system to autoimmune diabetes: a role for the CR1/CR2 complement receptors.
70	10433799	The complement component of the innate immune system regulates B cell activation and tolerance through complement receptors CR1/CR2.
71	10433799	Examination of the lymphoid compartments of NOD mice revealed striking expansion of a splenic B cell subset with high cell surface expression of CR1/CR2.
72	10433799	Importantly, long-term in vivo blockade of C3 binding to CR1/CR2 prevented the emergence of the CR1/CR2(hi) B cells and afforded resistance to autoimmune diabetes in NOD mice.
73	10806782	The results showed that before treatment the level of serum zinc and red cell C3b receptor rosette(RBCK-C3b RR), T-lymphocyte subgroup CD3, CD4, and CD4/CD8 were decreased(P < 0.01), while CD8, red cell immune complex rosette(RBC-ICR) were increased.
74	10806782	After treatment with zinc gluconate for 1 month the serum zinc level, RBC-C3b RR, RBC-ICR, CD3 and CD4/CD8 became normal, CD8 also approached to normal.
75	12445729	In some disease states such as systemic lupus erythematosus (SLE), acquired immune deficiency syndrome (AIDS), insulin-dependent diabetes mellitus and malaria, erythrocyte CR1 levels are reduced and CR1 function may be impaired.
76	20134434	Simultaneous detection of up to eight colors is enabled by careful selection and testing of cell-subset-defining monoclonal antibodies (anchor markers) in the appropriate fluorochrome combinations, in order to show the quantification of surface expression levels of molecules involved in chemotaxis (e.g., CX(3)CR1 and CCR2), adhesion (e.g., CD11b and CD62L), antigen presentation (e.g., CD83, CD86 and CD209) and immune regulation (e.g., CD101) on circulating APCs.
77	21459435	In this study, human soluble complement receptor 1 (sCR1) was immobilized on the islet cell surface through poly(ethylene glycol)-conjugated phospholipid (PEG-lipid) without loss of islet cell viability or insulin secretion ability. sCR1 on islets effectively inhibits complement activation and protects islets against attack by xenoreactive antibodies and complement.