共查询到12条相似文献,搜索用时 15 毫秒
1.
M. Oimomi F. Hata N. Igaki T. Nakamichi S. Baba H. Kato 《Cellular and molecular life sciences : CMLS》1989,45(5):463-466
Summary Alfa-ketoaldehyde dehydrogenase, which was extracted and purified from human livers, may act on carbonyl compounds, such as 3-deoxyglucosone, and be involved in the control of glycation (Maillard reaction) in the body. 相似文献
2.
A. G. Bosanquet A. M. Chandler A. H. Gordon 《Cellular and molecular life sciences : CMLS》1976,32(10):1348-1349
Summary The effects of injury on the concentration of 1-macroglobulin and 2-macroglobulin in the plasmas of male and female rats has been investigated. At 5 days after injury to the male rats the 1-macroglobulin concentration increased to 131% of its preinjury value. The 2-macroglobulin concentration increased more rapidly to a maximum of 86 times its initial value. In the female rats 2-macroglobulin increased only slightly and 1-macroglobulin not at all. 相似文献
3.
Endomannosidase processes oligosaccharides of α1-antitrypsin and its naturally occurring genetic variants in the Golgi apparatus 总被引:3,自引:0,他引:3
Torossi T Fan JY Sauter-Etter K Roth J Ziak M 《Cellular and molecular life sciences : CMLS》2006,63(16):1923-1932
Endomannosidase provides an alternate glucose-trimming pathway in the Golgi apparatus. However, it is unknown if the action
of endomannosidase is dependent on the conformation of the substrate. We have investigated the processing by endomannosidase
of the α1-antitrypsin oligosaccharides and its disease-causing misfolded Z and Hong Kong variants. Oligosaccharides of wild-type
and misfolded α1-antitrypsin expressed in castanospermine-treated hepatocytes or glucosidase II-deficient Phar 2.7 cells were
selectively processed by endomannosidase and subsequently converted to complex type oligosaccharides as indicated by Endo
H resistance and PNGase F sensitivity. Overexpression of endomannosidase in castanospermine-treated hepatocytes resulted in
processing of all oligosaccharides of wild-type and variants of α1-antitrypsin. Thus, endomannosidase does not discriminate
the folding state of the substrate and provides a back-up mechanism for completion of N-glycosylation of endoplasmic reticulum-escaped glucosylated glycoproteins. For exported misfolded glycoproteins, this would
provide a pathway for the formation of mature oligosaccharides important for their proper trafficking and correct functioning.
Received 18 April 2006; received after revision 12 June 2006; accepted 15 June 2006 相似文献
4.
5.
Yasmina Manso Javier Carrasco Gemma Comes Paul A. Adlard Ashley I. Bush Juan Hidalgo 《Cellular and molecular life sciences : CMLS》2012,69(21):3665-3681
Alzheimer’s disease (AD) is by far the most commonly diagnosed dementia, and despite multiple efforts, there are still no effective drugs available for its treatment. One strategy that deserves to be pursued is to alter the expression and/or physiological action of endogenous proteins instead of administering exogenous factors. In this study, we intend to characterize the roles of the antioxidant, anti-inflammatory, and heavy-metal binding proteins, metallothionein-1?+?2 (MT1?+?2), in a mouse model of Alzheimer’s disease, Tg2576 mice. Contrary to expectations, MT1?+?2-deficiency rescued partially the human amyloid precursor protein-induced changes in mortality and body weight in a gender-dependent manner. On the other hand, amyloid plaque burden was decreased in the cortex and hippocampus in both sexes, while the amyloid cascade, neuroinflammation, and behavior were affected in the absence of MT1?+?2 in a complex manner. These results highlight that the control of the endogenous production and/or action of MT1?+?2 could represent a powerful therapeutic target in AD. 相似文献
6.
E. F. Lüscher 《Cellular and molecular life sciences : CMLS》1956,12(7):268-270
Zusammenfassung Die visköse Metamorphose der Blutplättchen ist ein von der Fibrinbildung unabhängiger Prozess, der durch Thrombin und einen thermostabilen, dialysierbaren Faktor aus Plasma oder Serum ausgelöst wird. Das unter diesen Bedingungen aus den zerfallenden Plättchen austretende Material kontrahiert sich spontan. Dies erklärt die Gerinnselretraktion, bei der dem Fibrin folglich eine völlig passive Rolle zukommt.
Supported by grants from the Swiss National Foundation for Scientific Research and the F. Hoffmann-La Roche Foundation. 相似文献
Supported by grants from the Swiss National Foundation for Scientific Research and the F. Hoffmann-La Roche Foundation. 相似文献
7.
F. E. Weber J. H. Dyer F. López García M. Werder T. Szyperski K. Wüthrich H. Hauser 《Cellular and molecular life sciences : CMLS》1998,54(7):751-759
The preform of the rabbit sterol carrier protein 2 (pre-rSCP2) was cloned, the uniformly 15N-labelled protein expressed in Escherichia coli and studied by three-dimensional 15N-resolved nuclear magnetic resonance spectroscopy. In spite of its low solubility in aqueous solution of only ∼0.3 mM, sequential
15N and 1H backbone resonance assignments were obtained for 105 out of the 143 residues. From comparison of the sequential and medium-range
nuclear Overhauser effects (NOEs) in the two proteins, all regular secondary structures previously determined in mature human
SCP2 (hSCP2) [Szyperski et al. (1993) FEBS Lett. 335: 18–26] were also identified in pre-rSCP2. Near-identity of the backbone 15N and 1H chemical shifts and 1 : 1 correspondence of 24 long-range NOEs to backbone amide groups in the two proteins show that the
residues 21 – 143 adopt the same globular fold in pre-rSCP2 and mature hSCP2. The N-terminal 20-residue leader peptide of pre-rSCP2 is flexibly disordered in solution and does not observably affect the conformation of the polypeptide segment 21 – 143.
Received 11 May 1998; accepted 15 May 1998 相似文献
8.
Zusammenfassung Bei chinesischen Hamstern aus Inzuchten mit erblicher Zuckerkrankheit wurden erhöhte Serum--2-Eiweisswerte konstatiert. Die Erhöhung erfolgt vor Auftreten der Hyperglykämie oder Blutgefäss- und anderen sekundären pathologischen Veränderungen. Es wird gefolgert, dass die Eiweisserhöhung gen-bedingt ist und wahrscheinlich chemisch abnormales Eiweiss betrifft.
This investigation was supported in part by research grants from the National Institutes of Health, USPHS #E1560 and #CY3335, the National Science Foundation (#6-9602), and the Damon Runyon Memorial Fund (#293). 相似文献
This investigation was supported in part by research grants from the National Institutes of Health, USPHS #E1560 and #CY3335, the National Science Foundation (#6-9602), and the Damon Runyon Memorial Fund (#293). 相似文献
9.
An increase in the concentration of cytosolic free Ca2+ is a key component regulating different cellular processes ranging from egg fertilization, active secretion and movement,
to cell differentiation and death. The multitude of phenomena modulated by Ca2+, however, do not simply rely on increases/decreases in its concentration, but also on specific timing, shape and sub-cellular
localization of its signals that, combined together, provide a huge versatility in Ca2+ signaling. Intracellular organelles and their Ca2+ handling machineries exert key roles in this complex and precise mechanism, and this review will try to depict a map of Ca2+ routes inside cells, highlighting the uniqueness of the different Ca2+ toolkit components and the complexity of the interactions between them. 相似文献
10.
Bartolomé F de Las Cuevas N Muñoz U Bermejo F Martín-Requero A 《Cellular and molecular life sciences : CMLS》2007,64(11):1437-1448
We have analyzed the intracellular signals that allow lymphoblasts from Alzheimer’s disease (AD) patients to escape from serum
deprivation-induced apoptosis. The following observations suggested that modulation of ERK1/2 activity by Ca2+/calmodulin (CaM) is involved in preventing apoptosis: (i) ERK1/2 activity seems to support lethality in control cells, as
PD98059, the inhibitor of the activating MEK prevented cell death; (ii) control cells show a persistent and higher stimulation
of ERK1/2 than that of AD cells in the absence of serum; (iii) CaM antagonists have no effects on control cells, but sensitize
AD cells to death induced by serum withdrawal and increased ERK1/2 phosphorylation, and (iv) no apoptotic effects of CaM antagonists
were observed in AD cells treated with PD98059. These results suggest the existence of an activation threshold of the ERK1/2
pathway setting by Ca2+/CaM-dependent mechanisms, which appears to be the critical factor controlling cell survival or death decision under trophic
factor withdrawal.
F. Bartolomé, N. de las Cuevas: These authors contributed equally to this work.
Received 14 February 2007; received after revision 16 April 2007; accepted 23 April 2007 相似文献
11.
12.
Hailey–Hailey disease (HHD) is a rare autosomal dominant acantholytic dermatosis, characterized by a chronic course of repeated and exacerbated skin lesions in friction regions. The pathogenic gene of HHD was reported to be the ATPase calcium-transporting type 2C member 1 gene (ATP2C1) located on chromosome 3q21–q24. Its function is to maintain normal intracellular concentrations of Ca2+/Mn2+ by transporting Ca2+/Mn2+ into the Golgi apparatus. ATP2C1 gene mutations are reportedly responsible for abnormal cytosolic Ca2+/Mn2+ levels and the clinical manifestations of HHD. Environmental factors and genetic modifiers may also affect the clinical variability of HHD. This article aims to critically discuss the clinical and pathological features of HHD, differential diagnoses, and genetic and functional studies of the ATP2C1 gene in HHD. Further understanding the role of the ATP2C1 gene in the pathogenesis of HHD by genetic, molecular, and animal studies may contribute to a better clinical diagnosis and provide new strategies for the treatment and prevention of HHD. 相似文献