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排序方式: 共有87条查询结果,搜索用时 15 毫秒
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C Allard V Desgagné J Patenaude M Lacroix L Guillemette MC Battista M Doyon J Ménard JL Ardilouze P Perron L Bouchard MF Hivert 《Epigenetics》2015,10(4):342-351
Leptin is an adipokine that acts in the central nervous system and regulates energy balance. Animal models and human observational studies have suggested that leptin surge in the perinatal period has a critical role in programming long-term risk of obesity. In utero exposure to maternal hyperglycemia has been associated with increased risk of obesity later in life. Epigenetic mechanisms are suspected to be involved in fetal programming of long term metabolic diseases. We investigated whether DNA methylation levels near LEP locus mediate the relation between maternal glycemia and neonatal leptin levels using the 2-step epigenetic Mendelian randomization approach. We used data and samples from up to 485 mother-child dyads from Gen3G, a large prospective population-based cohort. First, we built a genetic risk score to capture maternal glycemia based on 10 known glycemic genetic variants (GRS10) and showed it was an adequate instrumental variable (β = 0.046 mmol/L of maternal fasting glucose per additional risk allele; SE = 0.007; P = 7.8 × 10−11; N = 467). A higher GRS10 was associated with lower methylation levels at cg12083122 located near LEP (β = −0.072 unit per additional risk allele; SE = 0.04; P = 0.05; N = 166). Direction and effect size of association between the instrumental variable GRS10 and methylation at cg12083122 were consistent with the negative association we observed using measured maternal glycemia. Lower DNA methylation levels at cg12083122 were associated with higher cord blood leptin levels (β = −0.17 log of cord blood leptin per unit; SE = 0.07; P = 0.01; N = 170). Our study supports that maternal glycemia is part of causal pathways influencing offspring leptin epigenetic regulation. 相似文献
33.
R Einspanier A Einspanier F Wempe K H Scheit 《Biochemical and biophysical research communications》1991,179(2):1006-1010
A new acidic seminal fluid protein (aSFP) was purified from bovine seminal fluid, using anion exchange chromatography and FPLC on MonoQ. The purified aSFP displays a pI of 4.8 and an apparent molecular weight of 14 kDa. Homogeneity of aSFP was demonstrated by FPLC and SDS-polyacrylamide gel electrophoresis. Monospecific anti-aSFP IgGs were employed to characterize aSFP in bovine seminal plasma and seminal vesicle secretion by immuno blot analysis. Proteinchemical characterization of aSFP included amino acid analysis as well as determination of 23 amino acid residues of the N-terminal sequence of aSFP. According to this sequence, aSFP appears to represent a hitherto unknown protein. aSFP stimulated cell division and progesterone secretion of bovine granulosa cells in vitro in a potent and dose dependent manner. aSFP appears to be a potent growth factor with effects on ovarian granulosa cells. 相似文献
34.
G Rapp J Freudenstein J Klaudiny J Mucha F Wempe M Zimmer K H Scheit 《DNA and cell biology》1990,9(7):479-485
35.
F Wempe S Wagner H vd Kammer E Krauhs K H Scheit 《Biochimica et biophysica acta》1990,1034(3):260-262
From the experimental results of three independent methods: (1) indirect immunofluorescence employing monospecific anti-seminalplasmin-IgGs, (2) cell-free translation of poly(A)+ RNA from seminal vesicle and testicular tissue, as well as (3) Northern analysis of poly(A)+ RNA of the latter tissues with a synthetic seminalplasmin-specific antisense DNA probe, it is concluded that the biosynthesis of seminalplasmin occurs in seminal vesicles but not in testis. 相似文献
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A recent insertion of an alu element on the Y chromosome is a useful marker for human population studies 总被引:23,自引:2,他引:21
A member of the Alu family of repeated DNA elements has been identified on
the long arm of the human Y chromosome, Yq11. This element, referred to as
the Y Alu polymorphic (YAP) element, is present at a specific site on the Y
chromosome in some humans and is absent in others. Phylogenetic comparisons
with other Alu sequences reveal that the YAP element is a member of the
polymorphic subfamily-3 (PSF-3), a previously undefined subfamily of Alu
elements. The evolutionary relationships of PSF-3 to other Alu subfamilies
support the hypothesis that recently inserted elements result from multiple
source genes. The frequency of the YAP element is described in 340
individuals from 14 populations, and the data are combined with those from
other populations. There is both significant heterogeneity among
populations and a clear pattern in the frequencies of the insertion:
sub-Saharan Africans have the highest frequencies, followed by northern
Africans, Europeans, Oceanians, and Asians. An interesting exception is the
relatively high frequency of the YAP element in Japanese. The greatest
genetic distance is observed between the African and non-African
populations. The YAP is especially useful for studying human population
history from the perspective of male lineages.
相似文献
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Promsuk Jutabha Naohiko Anzai Kenichiro Kitamura Atsuo Taniguchi Shuji Kaneko Kunimasa Yan Hideomi Yamada Hidetaka Shimada Toru Kimura Tomohisa Katada Toshiyuki Fukutomi Kimio Tomita Wako Urano Hisashi Yamanaka George Seki Toshiro Fujita Yoshinori Moriyama Akira Yamada Shunya Uchida Michael F. Wempe Hitoshi Endou Hiroyuki Sakurai 《The Journal of biological chemistry》2010,285(45):35123-35132
The evolutionary loss of hepatic urate oxidase (uricase) has resulted in humans with elevated serum uric acid (urate). Uricase loss may have been beneficial to early primate survival. However, an elevated serum urate has predisposed man to hyperuricemia, a metabolic disturbance leading to gout, hypertension, and various cardiovascular diseases. Human serum urate levels are largely determined by urate reabsorption and secretion in the kidney. Renal urate reabsorption is controlled via two proximal tubular urate transporters: apical URAT1 (SLC22A12) and basolateral URATv1/GLUT9 (SLC2A9). In contrast, the molecular mechanism(s) for renal urate secretion remain unknown. In this report, we demonstrate that an orphan transporter hNPT4 (human sodium phosphate transporter 4; SLC17A3) was a multispecific organic anion efflux transporter expressed in the kidneys and liver. hNPT4 was localized at the apical side of renal tubules and functioned as a voltage-driven urate transporter. Furthermore, loop diuretics, such as furosemide and bumetanide, substantially interacted with hNPT4. Thus, this protein is likely to act as a common secretion route for both drugs and may play an important role in diuretics-induced hyperuricemia. The in vivo role of hNPT4 was suggested by two hyperuricemia patients with missense mutations in SLC17A3. These mutated versions of hNPT4 exhibited reduced urate efflux when they were expressed in Xenopus oocytes. Our findings will complete a model of urate secretion in the renal tubular cell, where intracellular urate taken up via OAT1 and/or OAT3 from the blood exits from the cell into the lumen via hNPT4. 相似文献