scholarly journals Complement Factor H Gene Abnormalities in Haemolytic Uraemic Syndrome: From Point Mutations to Hybrid Gene

PLoS Medicine ◽  
2006 ◽  
Vol 3 (10) ◽  
pp. e432 ◽  
Author(s):  
Marina Noris ◽  
Giuseppe Remuzzi
2017 ◽  
Vol 10 (2) ◽  
pp. 263-265
Author(s):  
James Collett ◽  
Amali Mallawaarachchi ◽  
Eddy Fischer ◽  
Muralikrishna Gangadharan Komala ◽  
Kamal Sud ◽  
...  

2017 ◽  
Vol 135 (10) ◽  
pp. 1037 ◽  
Author(s):  
Eveline Kersten ◽  
Maartje J. Geerlings ◽  
Anneke I. den Hollander ◽  
Eiko K. de Jong ◽  
Sascha Fauser ◽  
...  

2000 ◽  
Vol 66 (5) ◽  
pp. 1721-1722 ◽  
Author(s):  
Mark R.H. Buddles ◽  
Rosemary L. Donne ◽  
Anna Richards ◽  
Judith Goodship ◽  
Timothy H.J. Goodship

2003 ◽  
Vol 12 (24) ◽  
pp. 3385-3395 ◽  
Author(s):  
Jessica Caprioli ◽  
Federica Castelletti ◽  
Sara Bucchioni ◽  
Paola Bettinaglio ◽  
Elena Bresin ◽  
...  

2016 ◽  
Vol 64 ◽  
pp. 123-129 ◽  
Author(s):  
Xuan Liao ◽  
Chang-Jun Lan ◽  
Isabella-Wai-Yin Cheuk ◽  
Qing-qing Tan

2007 ◽  
Vol 44 (16) ◽  
pp. 3968
Author(s):  
Gábor Széplaki ◽  
Tímea Gombos ◽  
Bernadett Blaskó ◽  
Adrienn Bíró ◽  
Zsófia Bánlaki ◽  
...  

2007 ◽  
Vol 113 (4) ◽  
pp. 213-218 ◽  
Author(s):  
Klaus Stark ◽  
Katharina Neureuther ◽  
Kamil Sedlacek ◽  
Wibke Hengstenberg ◽  
Marcus Fischer ◽  
...  

Recently, the genetic variant Y402H in the CFH (complement factor H) gene was associated with an increased risk for MI (myocardial infarction) in a prospective Caucasian cohort. In another nested case-control study, however, the CFH-Y402H variant did not carry susceptibility to MI. The aim of the present study was to test for an association between the CFH-Y402H variant and MI in a large case-control sample with a familial background for CAD (coronary artery disease). A total of 2161 individuals from the German MI family study were studied by questionnaire, physical examination and biochemical analyses. MI patients (n=1188; 51.4±8.6 years at first MI) were recruited from families with at least two members affected by MI and/or severe CAD. Spouses, sisters-in-law and brothers-in-law respectively, without MI/CAD were included as unaffected controls (n=973; 56.9±9.8 years). Genotyping was performed using a TaqMan assay. The common Y402H variant in the CFH gene was not associated with classical cardiovascular risk factors (diabetes, hypercholesterolaemia, hypertension, obesity, smoking and C-reactive protein serum levels). No association was found between the CFH-Y402H variant and susceptibility to MI. Separate analyses in both men and women revealed no gender-specific influence of the gene variant on cardiovascular risk factors or MI. This investigation was unable to replicate the association between the common CFH-Y402H variant and susceptibility to MI in our large Caucasian population which is enriched for genetic factors. We conclude that the CFH-Y402H variant has no relevant risk-modifying effect in our population.


1997 ◽  
Vol 75 (5) ◽  
pp. 508-510 ◽  
Author(s):  
Helena M Ward ◽  
Naomi H Higgs ◽  
Timothy K Blackmore ◽  
Tania A Sadlon ◽  
David L Gordon

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