نتایج جستجو برای: incomplete penetrance

تعداد نتایج: 61081  

2016
Anna M. Rose Amna Z. Shah Giulia Venturini Abhay Krishna Aravinda Chakravarti Carlo Rivolta Shomi S. Bhattacharya

PRPF31-associated retinitis pigmentosa presents a fascinating enigma: some mutation carriers are blind, while others are asymptomatic. We identify the major molecular cause of this incomplete penetrance through three cardinal features: (1) there is population variation in the number (3 or 4) of a minisatellite repeat element (MSR1) adjacent to the PRPF31 core promoter; (2) in vitro, 3-copies of...

2014
Carla Giordano Luisa Iommarini Luca Giordano Alessandra Maresca Annalinda Pisano Maria Lucia Valentino Leonardo Caporali Rocco Liguori Stefania Deceglie Marina Roberti Francesca Fanelli Flavio Fracasso Fred N. Ross-Cisneros Pio D’Adamo Gavin Hudson Angela Pyle Patrick Yu-Wai-Man Patrick F. Chinnery Massimo Zeviani Solange R. Salomao Adriana Berezovsky Rubens Belfort Dora Fix Ventura Milton Moraes Milton Moraes Filho Piero Barboni Federico Sadun Annamaria De Negri Alfredo A. Sadun Andrea Tancredi Massimiliano Mancini Giulia d’Amati Paola Loguercio Polosa Palmiro Cantatore Valerio Carelli

Leber's hereditary optic neuropathy is a maternally inherited blinding disease caused as a result of homoplasmic point mutations in complex I subunit genes of mitochondrial DNA. It is characterized by incomplete penetrance, as only some mutation carriers become affected. Thus, the mitochondrial DNA mutation is necessary but not sufficient to cause optic neuropathy. Environmental triggers and ge...

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2012
William Cohen Christel Castelli Marie-Christine Alessi Marie-Françoise Aillaud Sophie Bouvet Noémie Saut Dominique Brunet Marie-Christine Barthet David-Alexandre Tregouet Géraldine Lavigne Pierre-Emmanuel Morange

OBJECTIVE We aimed to study the association among ABO blood group, von Willebrand factor, factor VIII plasma levels, and the risk of venous thrombosis (VT) in a cohort of 1774 relatives from 500 families with inherited thrombophilia. METHODS AND RESULTS One hundred sixty-one of the 1774 relatives had a VT. Different risk groups were formed: no, low-(factor V Leiden or F2G20210A heterozygous c...

Journal: :Archives of neurology 2006
Carles Gaig Mario Ezquerra Maria Jose Marti Esteban Muñoz Francesc Valldeoriola Eduardo Tolosa

BACKGROUND Several pathogenic mutations in the LRRK2 gene have been implicated in familial and sporadic cases of Parkinson disease (PD). The R1441G mutation is frequent in Spanish patients of Basque ethnicity with PD, and the G2019S mutation is a common mutation found in several populations worldwide. OBJECTIVES To determine the frequency of the LRRK2 G2019S and R1441G mutations in PD patient...

2012
Giulia Venturini Anna M. Rose Amna Z. Shah Shomi S. Bhattacharya Carlo Rivolta

Heterozygous mutations in the PRPF31 gene cause autosomal dominant retinitis pigmentosa (adRP), a hereditary disorder leading to progressive blindness. In some cases, such mutations display incomplete penetrance, implying that certain carriers develop retinal degeneration while others have no symptoms at all. Asymptomatic carriers are protected from the disease by a higher than average expressi...

Journal: :Investigative ophthalmology & visual science 2017
Nahid Akhtar Khan Periyasamy Govindaraj Nagasamy Soumittra Sonika Sharma Sundaramoorthy Srilekha Selvakumar Ambika Ayyasamy Vanniarajan Angamuthu Kanikannan Meena Megha S Uppin Challa Sundaram Parayil Sankaran Bindu Narayanappa Gayathri Arun B Taly Kumarasamy Thangaraj

Purpose Leber's hereditary optic neuropathy (LHON; OMIM 535000) is one of the most common maternally inherited mitochondrial disorders. Three mitochondrial DNA point mutations-m.3460G>A (MT-ND1), m.11778G>A (MT-ND4), and m.14484T>C (MT-ND6)-account for the majority of reported LHON cases. Only approximately 50% of males and approximately 10% of females carrying these mutations develop optic neu...

Journal: :Journal of the American Society of Nephrology : JASN 2013
Elena Bresin Erica Rurali Jessica Caprioli Pilar Sanchez-Corral Veronique Fremeaux-Bacchi Santiago Rodriguez de Cordoba Sheila Pinto Timothy H J Goodship Marta Alberti David Ribes Elisabetta Valoti Giuseppe Remuzzi Marina Noris

Several abnormalities in complement genes reportedly contribute to atypical hemolytic uremic syndrome (aHUS), but incomplete penetrance suggests that additional factors are necessary for the disease to manifest. Here, we sought to describe genotype-phenotype correlations among patients with combined mutations, defined as mutations in more than one complement gene. We screened 795 patients with ...

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