Complement Factor H-Related 5 (CFHR5) ELISA Kits

Human Complement Factor H-Related 5 (CFHR5) interaction partners

1. Higher circulating FHR-5 levels in IgA nephropathy patients were associated with a lower estimated glomerular filtration rate, hypertension, and severe Oxford-T and Oxford-C scores. High FHR-5 levels were independently and significantly associated with a risk of developing either a 30% decline in the estimated glomerular filtration rate or end-stage renal disease.

2. Novel genetic rearrangement generated from a heterozygous deletion spanning 146 Kbp involving multiple CFHR genes leading to a CFHR1-R5 hybrid protein. This deletion was found in four family members presenting with a familial dominant glomerulopathy.

3. Higher serum FHR-5 levels were associated with a lack of response to immunosuppression, the presence of endocapillary hypercellularity, and histology scores of IgA nephropathy severity.

4. Our study found that rare variants in CFHR5 may contribute to the genetic susceptibility to IgA Nephropathy, which suggests that CFHR5 is an IgA Nephropathy susceptibility gene

5. Next-generation sequencing of the CFH region identified putatively functional variants (missense, splice site and indel) on the four common haplotypes. We found no expression of any of the five CFH-related genes in the retina or RPE/Choroid/Sclera, in contrast to the liver, which is the main source of the circulating proteins. [CFHR5]

6. Studies indicate that complement factor H-related proteins (FHR1-5) may enhance complement activation, with important implications for the role of these proteins in disease.

7. In this study, we identify pentraxin 3 (PTX3) as a novel ligand of CFHR5

8. At least two distinct intronic breakpoints within the CFHR5 gene can cause the same mutant CFHR5 protein and C3 glomerulopathy.

9. A hybrid CFHR2-CFHR5 plasma protein, arising from a chromosomal deletion mutation stabilizes the C3 convertase and reduces factor H-mediated convertase decay.

10. Recent investigations in London and Cyprus culminated in the identification of another autosomal dominant condition that presents with microscopic haematuria because of heterozygous mutations in the CFHR5 gene--{review}

11. A potentially pathogenic sequence variation was found in CFHR5 in the patients with atypical hemolytic uremic syndrome.

12. CFHR5 nephropathy is discussed.

13. Describe the clinical course, significant variable expressivity, and marked gender difference regarding the development of chronic renal failure in familial C3 glomerulopathy associated with CFHR5 mutations.

14. evidence for an inherited renal disease, endemic in Cyprus, characterised by microscopic and synpharyngitic macroscopic haematuria, renal failure and C3 glomerulonephritis; affected individuals have an internal duplication within the gene for CFHR5

15. Study identified novel mutations in CFH, CFHR5, CFI, CFB and C3 in American patients with atypical hemolytic uremic syndrome.

16. Maps to between FHR-2 and the non-complement protein factor XIIIb at 1q32.

17. FHR-5 shares properties of binding heparin and C-reactive protein and lipoprotein association with one or more of the other FHRs, but is unique among this family of proteins in possessing independent complement-regulatory activity.

18. Identification of specific variants of variants of CFHR5 in membranoproliferative glomerulonephritis type II.

19. CFHR5 genetic alterations may play a secondary role in the pathogenesis of haemolytic uraemic syndrome.

20. No definitive pathogenic CFHR5 mutations have been found in any of 639 unrelated patients with age-related macular degeneration (AMD), indicating that sequence variations in CFHR5 do not play a major role in determining AMD susceptibility.