نتایج جستجو برای: missense

تعداد نتایج: 12396  

2015
E Forsythe K Sparks BE Hoskins E Bagkeris BM McGowan PV Carroll MSB Huda S Mujahid C Peters T Barrett S Mohammed PL Beales

Bardet-Biedl syndrome is a rare ciliopathy characterized by retinal dystrophy, obesity, intellectual disability, polydactyly, hypogonadism and renal impairment. Patients are at high risk of cardiovascular disease. Mutations in BBS1 and BBS10 account for more than half of those with molecular confirmation of the diagnosis. To elucidate genotype-phenotype correlations with respect to cardiovascul...

2014
Lucy Gossage Douglas E. V. Pires Álvaro Olivera-Nappa Juan Asenjo Mark Bycroft Tom L. Blundell Tim Eisen

Mutations in the von Hippel-Lindau (VHL) gene are pathogenic in VHL disease, congenital polycythaemia and clear cell renal carcinoma (ccRCC). pVHL forms a ternary complex with elongin C and elongin B, critical for pVHL stability and function, which interacts with Cullin-2 and RING-box protein 1 to target hypoxia-inducible factor for polyubiquitination and proteasomal degradation. We describe a ...

Journal: :Journal of the American College of Cardiology 1998
Y Shimasaki H Yasue M Yoshimura M Nakayama K Kugiyama H Ogawa E Harada T Masuda W Koyama Y Saito Y Miyamoto Y Ogawa K Nakao

OBJECTIVES We examined the possible association between the missense Glu298Asp variant of the endothelial nitric oxide synthase (eNOS) gene and myocardial infarction (MI). BACKGROUND Endothelium-derived nitric oxide (NO) plays a key role in the regulation of vascular tone. Recently, we reported that a missense Glu298Asp variant in exon 7 of the eNOS gene is a possible genetic factor involved ...

Journal: :Cancer research 1999
S Kato A Shimada M Osada S Ikawa M Obinata A Nakagawara R Kanamaru C Ishioka

The p51/p63 gene is a homologue of p53, the product of which acts as a transcriptional activator by binding to p53-responsive elements in the promoter regions of several p53 downstream genes. Recently, we identified four distinct mutations in the p51/p63 gene after screening >200 human tumors and cell lines. Because all of the detected p51/p63 mutations were missense mutations, the pathogenic e...

2005
Rodney J Scott Cliff J Meldrum

In the analysis of genes associated with predispositions to malignancy the causative status of mutations can be made relatively easily where it is obvious that there is a clear disruption in the coding sequence of the gene. Difficulties arise, however, if missense mutations are identified, as these are not easily categorised into genetic variants that are not associated with disease risk or int...

Journal: :The American Journal of Human Genetics 2010

Journal: :The American Journal of Human Genetics 2005

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2015
Lisa A Miosge Matthew A Field Yovina Sontani Vicky Cho Simon Johnson Anna Palkova Bhavani Balakishnan Rong Liang Yafei Zhang Stephen Lyon Bruce Beutler Belinda Whittle Edward M Bertram Anselm Enders Christopher C Goodnow T Daniel Andrews

Each person's genome sequence has thousands of missense variants. Practical interpretation of their functional significance must rely on computational inferences in the absence of exhaustive experimental measurements. Here we analyzed the efficacy of these inferences in 33 de novo missense mutations revealed by sequencing in first-generation progeny of N-ethyl-N-nitrosourea-treated mice, involv...

Journal: :Cancer research 2006
Nicholas P Taylor Matthew A Powell Randall K Gibb Janet S Rader Phyllis C Huettner Stephen N Thibodeau David G Mutch Paul J Goodfellow

MLH3 is a recently described member of the DNA mismatch repair gene family. Based on its interaction with the MutL homologue MLH1, it was postulated that MLH3 might play a role in tumorigenesis. Germ line and somatic mutations in MLH3 have been identified in a small fraction of colorectal cancers, but the role of MLH3 in colorectal cancer tumorigenesis remains controversial. We investigated MLH...

2015
Shirou Tsuchida Akihiro Osaka Yuya Abe Naoya Hamaue Takashi Aoki

d-bifunctional protein (d-BP) deficiency is thought to lead to severe lipid metabolism disorders. To investigate the effect of naturally occurring missense mutations in the hydratase domain in d-BP, we constructed several d-BP hydratase variants and measured their activities. Missense mutations at sites whose conservation rates among 30 eukaryotes were < 70% did not affect hydratase activity. W...

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