The effect of CPT1B gene on lipid metabolism and its polymorphism analysis in Chinese Simmental cattle

2021 ◽  
pp. 1-13
Author(s):  
Wei He ◽  
Ming Gao ◽  
Runjun Yang ◽  
Zhihui Zhao ◽  
Jiaqi Mi ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Polymorphism Analysis ◽  
Simmental Cattle ◽  
Its Polymorphism

scholarly journals Expression of candidate genes of lipid metabolism in the Kazakhstani breeding simmental cattle

2017 ◽  
Vol 15 (4) ◽  
pp. 443-446 ◽  
Author(s):  
Toktar Bеkseitov ◽  
Rustem Аbeldinov ◽  
Tolegen Asanbaev ◽  
Gulnara Dzhaksybaeva
Keyword(s):  
Lipid Metabolism ◽  
Candidate Genes ◽  
Simmental Cattle

scholarly journals Molecular divergence of locally grown pumpkin (Cucurbita maxima) cultivars through some isozyme tests

2012 ◽  
Vol 19 ◽  
pp. 89-93
Author(s):  
ME Haque ◽  
MA Islam ◽  
B Sikdar
Keyword(s):  
Alkaline Phosphatase ◽  
Acid Phosphatase ◽  
Genetic Polymorphism ◽  
Malate Dehydrogenase ◽  
Polymorphism Analysis ◽  
Cucurbita Maxima ◽  
Extraction Buffer ◽  
Locally Grown ◽  
Its Polymorphism ◽  
Phosphatase Alkaline

Context: Pumpkin (Cucurbita maxima) is highly polymorphic vegetable species and its polymorphism can be analyzed by isozyme molecular marker. Objective: To analyze genetic polymorphism among 10 locally grown pumpkin cultivars by isozyme. Materials and Methods: Fresh leaves of young plant of different cultivars were used for enzyme extraction. Enzyme extracts were prepared by homogenizing of 2 g sample of each cultivar. Prechilled mortar and pestle nestled in ice along with 1% polyvinylpyrrolidone and 2 ml of chilled extraction buffer were used prior to centrifuge. N-PAGE was conducted for different isozymes and stained the gels with specific chemicals for band development. Results: Five isozymes (peroxidase, esterase, acid phosphatase, alkaline phosphatase and malate dehydrogenase) were tested for genetic polymorphism analysis of pumpkin cultivars. Among them esterase, peroxidase and alkaline phosphatase showed polymorphism in different cultivars with 75-, 58.33- and 41.18% respectively. But acid phosphatase and malate dehydrogenase did not show any polymorphism. Esterase and peroxidase produced band quickly than others. Relative mobility of first band of esterase, peroxidase, acid phosphatase, alkaline phosphatase and malate deghdrogenase was 0.063, 0.045, 0.262, 0.07 and 0.093 respectively Conclusion: Out of five isozymes, effective polymorphism was found in esterase and peroxidase test DOI: http://dx.doi.org/10.3329/jbs.v19i0.13006 J. bio-sci. 19 89-93, 2011

A Cytochemical Study of Glucose-6-Phosphatase (G-6-PASE) in Cells Participating in Atherogenesis of Rabbit Aorta

1975 ◽  
Vol 33 ◽  
pp. 460-461
Author(s):  
Sidney D. Kobernick ◽  
Edna A. Elfont ◽  
Neddra L. Brooks
Keyword(s):  
Lipid Metabolism ◽  
New Zealand ◽  
Aortic Wall ◽  
Rabbit Aorta ◽  
Plaque Formation ◽  
Metabolic Changes ◽  
Atherosclerotic Plaques ◽  
Cytochemical Study ◽  
Cellular Alteration ◽  
New Zealand White Rabbits

This cytochemical study was designed to investigate early metabolic changes in the aortic wall that might lead to or accompany development of atherosclerotic plaques in rabbits. The hypothesis that the primary cellular alteration leading to plaque formation might be due to changes in either carbohydrate or lipid metabolism led to histochemical studies that showed elevation of G-6-Pase in atherosclerotic plaques of rabbit aorta. This observation initiated the present investigation to determine how early in plaque formation and in which cells this change could be observed.Male New Zealand white rabbits of approximately 2000 kg consumed normal diets or diets containing 0.25 or 1.0 gm of cholesterol per day for 10, 50 and 90 days. Aortas were injected jin situ with glutaraldehyde fixative and dissected out. The plaques were identified, isolated, minced and fixed for not more than 10 minutes. Incubation and postfixation proceeded as described by Leskes and co-workers.

Altered hepatic lipid metabolism in leptin-deficlent mice

2001 ◽  
Vol 120 (5) ◽  
pp. A546-A546
Author(s):  
D SWARTZBASILE ◽  
M GOLDBLATT ◽  
C SVATEK ◽  
M WALTERS ◽  
S CHOI ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid

The influence of the mental trauma on the behavior and lipid metabolism in female rats

2007 ◽  
Author(s):  
S. G. Tsikunov ◽  
A. G. Pshenichnaya ◽  
A. G. Kusov ◽  
N. N. Klyueva
Keyword(s):  
Lipid Metabolism ◽  
Female Rats ◽  
Mental Trauma

Ectopic Transcript Analysis Indicates that Allelic Exclusion is an Important Cause of Type I Protein C Deficiency in Patients with Nonsense and Frameshift Mutations in the PROC Gene

1996 ◽  
Vol 75 (06) ◽  
pp. 870-876 ◽  
Author(s):  
José Manuel Soria ◽  
Lutz-Peter Berg ◽  
Jordi Fontcuberta ◽  
Vijay V Kakkar ◽  
Xavier Estivill ◽  
...  
Keyword(s):  
Splice Site ◽  
Protein C ◽  
Stop Codon ◽  
Premature Stop Codon ◽  
Allelic Exclusion ◽  
Polymorphism Analysis ◽  
Type I ◽  
Protein C Deficiency ◽  
Nonsense Mutations ◽  
Stop Codons

SummaryNonsense mutations, deletions and splice site mutations are a common cause of type I protein C deficiency. Either directly or indirectly by altering the reading frame, these' lesions generate or may generate premature stop codons and could therefore be expected to result in premature termination of translation. In this study, the possibility that such mutations could instead exert their pathological effects at an earlier stage in the expression pathway, through “allelic exclusion” at the RNA level, was investigated. Protein C (PROC) mRNA was analysed in seven Spanish type I protein C deficient patients heterozygous for two nonsense mutations, a 7bp deletion, a 2bp insertion and three splice site mutations. Ectopic RNA transcripts from patient and control lymphocytes were analysed by RT-PCR and direct sequencing of amplified PROC cDNA fragments. The nonsense mutations and the deletion were absent from the cDNAs indicating that only mRNA derived from the normal allele had been expressed. Similarly for the splice site mutations, only normal PROC cDNAs were obtained. In one case, exclusion of the mutated allele could be confirmed by polymorphism analysis. In contrast to these six mutations, the 2 bp insertion was not associated with loss of mRNA from the mutated allele. In this case, cDNA analysis revealed the absence of 19 bases from the PROC mRNA consistent with the generation and utilization of a cryptic splice site 3’ to the site of mutation, which would result in a frameshift and a premature stop codon. It is concluded that allelic exclusion is a common causative mechanism in those cases of type I protein C deficiency which result from mutations that introduce premature stop codons

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