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1.
Multiple roles of the DSCR1 (Adapt78 or RCAN1) gene and its protein product Calcipressin 1 (or RCAN1) in disease 总被引:5,自引:0,他引:5
The DSCR1 (Adapt78) gene1 is transiently induced by stresses to temporarily protect cells against further potentially lethal challenges. However, chronic
expression of the DSCR1 (Adapt78) gene has now been implicated in several pathological conditions including Alzheimer’s disease, Down syndrome and cardiac
hypertrophy. Calcipressin 1 has been shown to function through direct binding and inhibition of the serine threonine protein
phosphatase Calcineurin. Pharmacological inhibition of calcineurin, by the immunosuppressive drugs cyclosporin A and FK506,
affects a wide variety of diseases. It is, therefore, likely that this endogenous calcineurin inhibitor, calcipressin 1, may
also play a role in a variety of human diseases.
1Please note that the mammalian DSCR1 gene is also called Adapt78 or RCAN1, and its protein products have been named Calcipressin1, MCIP1 and RCAN1. A proposal to adopt a single gene name of RCAN1 and a protein name RCAN1 (for Regulator of Calcineurin) has been endorsed by the HUGO Gene Nomenclature Committee, but final
approval must await agreement from a majority of researchers in the field.
Received 2 March 2005; received after revision 27 May 2005; accepted 19 July 2005 相似文献
2.
Cell-cell adhesion is a critical property of all multi-cellular organisms and its correct regulation is critical during development,
differentiation, tissue building and maintenance, and many immune responses. The multi-talin-like FERM domain containing protein,
FrmA, is required during starvation-induced multi-cellular development of Dictyostelium cells. Loss of FrmA leads to increased cell-cell adhesion and results in impaired multi-cellular development, slug migration
and fruiting bodies. Further, mixing experiments show that FrmA null cells are excluded from the apex of wild-type mounds,
to which cells that normally form the organising centre known as the tip sort. These data suggest a critical role for FrmA
in regulating cell-cell adhesion, multi-cellular development and, in particular, the formation of the organising centre known
as the tip.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.
Received 28 August 2008; received after revision 10 October 2008; accepted 21 October 2008 相似文献
3.
Carotenuto R De Marco N Biffo S Wilding M Vaccaro MC Marchisio PC Capriglione T Russo GL Campanella C 《Cellular and molecular life sciences : CMLS》2005,62(14):1641-1652
p27BBP/eIF6 is an evolutionarily conserved regulator of ribosomal function. It is necessary for 60S biogenesis and impedes improper joining of 40S and 60S subunits, regulated by protein kinase C or Efl1p. No data on p27BBP/eIF6 during early development of Metazoa are available. We studied the distribution, post-translational changes and association with the cytoskeleton of p27BBP/ eIF6 during Xenopus oogenesis and early development. Results indicate that p27BBP/eIF6 is present throughout oogenesis, partly associated with 60S subunits, partly free and with little cytoskeleton bound. During prophase I, p27BBP/eIF6 is detected as a single band of 27-kDa. Upon maturation induced by progesterone or protein kinase C, a serine-phosphorylated 29 kDa isoform appears and is kept throughout development to the neurula stage. Confocal microscopy showed that the distribution of p27BBP/eIF6 and its association with the cytoskeleton varies according to oogenesis stages. Briefly, in stage 6 oocytes, p27BBP/eIF6 has a limited dot-like distribution, and does not co-localize with cytokeratin, whereas upon maturation it spreads throughout the cytoplasm. After fertilization, a large fraction coalesces around cytomembranes and a cytochalasin B-sensitive co-localization with cytokeratin occurs. RNAse removes p27BBP/eIF6 from the cytokeratin fibres. Developmental data suggest a role of p27BBP/eIF6 in controlling ribosomal availability or regulating cross-talk between ribosomes and the cytoskeleton.Received 7 April 2005; received after revision 11 May 2005; accepted 25 May 2005R. Carotenuto and N. De Marco contributed equally to the paper 相似文献
4.
Transient receptor potential (TRP) ion channels have been identified as cellular sensors responding to diverse external and
internal stimuli. This review will cover the TRPV subfamily that comprises vertebrate and invertebrate members. The six mammalian
TRPV channels were demonstrated to function in thermosensation, mechanosensation, osmosensation and Ca2+ uptake. Invertebrate TRPV channels, five in Caenorhabditis elegans and two in Drosophila, have been shown to play a role in mechanosensation, such as hearing and proprioception in Drosophila and nose touch in C. elegans, and in the response to osmotic and chemical stimuli in C. elegans. We will focus here on the role that TRPV ion channels play in mechanosensation and a related sensory (sub-)modality, osmosensation.
Received 2 May 2005; received after revision 30 July 2005; accepted 30 August 2005 相似文献
5.
Protein-O-mannosyltransferases (Pmt proteins) catalyse the addition of mannose to serine or threonine residues of secretory proteins.
This modification was described first for yeast and later for other fungi, mammals, insects and recently also for bacteria.
O-mannosylation depends on specific isoforms of the three Pmt1, 2 and 4 subfamilies. In fungi, O-mannosylation determines the structure and integrity of cell walls, as well as cellular differentiation and virulence. O-mannosylation of specific secretory proteins of the human fungal pathogen Candida albicans and of the bacterial pathogen Mycobacterium tuberculosis contributes significantly to virulence. In mammals and insects, Pmt proteins are essential for cellular differentiation and
development, while lack of Pmt activity causes Walker-Warburg syndrome (muscular dystrophy) in humans. The susceptibility
of human cells to certain viruses may also depend on O-mannosyl chains. This review focuses on the various roles of Pmt proteins in cellular differentiation, development and virulence.
Received 6 September 2007; received after revision 3 October 2007; accepted 5 October 2007 相似文献
6.
Wittkopp PJ 《Cellular and molecular life sciences : CMLS》2005,62(16):1779-1783
Regulatory variation results from genetic changes with both cis and trans acting effects on gene expression. Here I describe the types of genetic variants that alter cis and trans regulation and discuss differences in the potential for cis and trans changes among different classes of genes. I argue that the molecular function of the protein encoded by each gene and how the gene is wired into the genomic regulatory network may influence its propensity for cis and trans regulatory changes.Received 15 February 2005; received after revision 12 April 2005; accepted 26 April 2005 相似文献
7.
Staphylococci have two mechanisms for resistance to β-lactam antibiotics. One is the production of β-lactamases, enzymes that
hydrolytically destroy β-lactams. The other is the expression of penicillin-binding protein 2a (PBP 2a), which is not susceptible
to inhibition by β-lactam antibiotics. Strains of S. aureus exhibiting either β-lactamase or PBP 2a-directed resistance (or both) have established a considerable ecological niche among
human pathogens. The emergence and subsequent spread of bacterial strains designated as methicillin-resistant S. aureus (MRSA), from the 1960s to the present, has created clinical difficulties for nosocomial treatment on a global scale. The
recent variants of MRSA that are resistant to glycopeptide antibiotics (such as vancomycin) have ushered in a new and disconcerting
chapter in the evolution of this organism.
Received 2 April 2005; received after revision 15 July 2005; accepted 25 July 2005 相似文献
8.
Inhibition of virus multiplication and alteration of cyclic AMP level in cell cultures by flavonoids
Summary The inhibitory effect of four flavonoid compounds on virus multiplication and their influence on the intracellular cyclic AMP (cAMP) level were studied in cell cultures. Quercetin and quercitrin reduced the yields ofHuman (alpha) herpesvirus 1 (HSV-1) andSuid (alpha) herpesvirus 1 (pseudorabies virus), but hesperidin and rutin had no effect. Further, quercetin and quercitrin elevated the intracellular level of cAMP, whereas hesperidin and rutin did not alter the cAMP level. Both antiviral activity and cAMP-enhancing effect were dependent on the concentrations of the flavonoids, and these effects turned out to be parallel.This study suggests that a relation exists between the antiviral effect and the cAMP-enhancing activity of flavonoids. 相似文献
9.
Y. X. Li J. Halloy J. L. Martiel B. Wurster A. Goldbeter 《Cellular and molecular life sciences : CMLS》1992,48(6):603-606
We investigate how the introduction of cells oscillating periodically affects the behaviour of a suspension ofDictyostelium discoideum amoebae undergoing chaotic oscillations of cyclic AMP. The analysis of a model indicates that a tiny proportion of periodic cells suffices to transform chaos into periodic oscillations in such suspensions. A similar result is obtained by forcing the aperiodic oscillations by a small-amplitude, periodic input of cyclic AMP. The results provide an explanation for the observation of regular oscillations in suspensions of a putatively chaotic mutant ofDictyostelium discoideum
12. More generally, the results show how chaos in biological systems may disappear through the coupling with periodic oscillations. 相似文献
10.
Biomedicine and diseases: the Klippel-Trenaunay syndrome, vascular anomalies and vascular morphogenesis 总被引:2,自引:0,他引:2
Vascular morphogenesis is a vital process for embryonic development, normal physiologic conditions (e.g. wound healing) and pathological processes (e.g. atherosclerosis, cancer). Genetic studies of vascular anomalies have led to identification of critical genes involved in vascular morphogenesis. A susceptibility gene, VG5Q (formally named AGGF1), was cloned for Klippel-Trenaunay syndrome (KTS). AGGF1 encodes a potent angiogenic factor, and KTS-associated mutations enhance angiogenic activity of AGGF1, defining ‘increased angiogenesis’ as one molecular mechanism for the pathogenesis of KTS. Similar studies have identified other genes involved in vascular anomalies as important genes for vascular morphogenesis, including TIE2, VEGFR-3, RASA1, KRIT1, MGC4607, PDCD10, glomulin, FOXC2, NEMO, SOX18, ENG, ACVRLK1, MADH4, NDP, TIMP3, Notch3, COL3A1 and PTEN. Future studies of vascular anomaly genes will provide insights into the molecular mechanisms for vascular morphogenesis, and may lead to the development of therapeutic strategies for treating these and other angiogenesis-related diseases, including coronary artery disease and cancer.Received 24 November 2004; received after revision 21 January 2005; accepted 2 March 2005 相似文献
11.
A. Oren 《Cellular and molecular life sciences : CMLS》1993,49(6-7):518-522
In the thirteen years of quantitative studies on the microbiology of the Dead Sea from 1980 onwards three distinct periods can be discerned. Mass development of the green unicellular algaDunaliella parva (up to 8,800 cells/ml) and red archaeobacteria (2×107 cells/ml) was observed in 1980, following a dilution of the upper water layers by rain floods. This bloom disappeared at the end of 1982 as a result of a complete mixing of the water column. During the period 1983–1991 the lake was holomictic, and noDunaliella cells were observed. Viable bacteria were present during this period in very low numbers. Heavy rain floods during the winter of 1991–1992 caused a new stratification as the upper five meters of the water column became diluted to 70% of their normal salinity. In this upper water layerDunaliella reappeared (up to 3×104 cells/ml at the beginning of May, rapidly declining to less than 40 cells/ml at the end of July), and a bloom of red archaeobacteria (3×107 cells/ml) once more imparted a red coloration to the lake. 相似文献
12.
Golgi-endomannosidase provides an alternate glucosidase-independent pathway of glucose trimming. Activity for endomannosidase
is detectable in various tissues and cell lines but not in CHO cells. Cloning of CHO cell endomannosidase revealed that the
highly conserved Trp188 and Arg177 of vertebrate endomannosidase were both substituted by Cys. The Trp188Cys substitution
was functionally important since it alone resulted in endoplasmic reticulum (ER) mislocalization of endomannosidase and caused
the greatly reduced in vivo activity. These effects could be reversed in cells with a back-engineered Cys188Trp CHO cell endomannosidase, in particular
N-glycans of α1-antitrypsin became fully processed. The intramolecular disulfide bridge of CHO cell endomannosidase formed
with the additional Cys188 was not solely responsible for the reduced enzyme activity since endomannosidase with engineered
Cys188Ala or Ser substitutions did not restore enzyme activity and was ER mislocalized. Thus, the conserved Trp188 residue
in endomannosidases is of critical importance for correct subcellular localization and in vivo activity of the enzyme.
Received 7 May 2007; received after revision 31 May 2007; accepted 11 June 2007 相似文献
13.
Matin A 《Cellular and molecular life sciences : CMLS》2007,64(11):1317-1322
The 129 mouse strain develops congenital testicular germ cell tumors (TGCTs) at a low frequency. TGCTs in mice resemble the
testicular tumors (teratomas) that occur in human infants. The genes that cause these tumors in 129 have not been identified.
The defect at the Ter locus increases TGCT incidence such that 94% of 129-Ter/Ter males develop TGCTs. The primary effect of the Ter mutation is progressive loss of primordial germ cells (PGCs) during embryonic development. This results in sterility in adult
Ter/Ter mice on all mouse strain backgrounds. However, on the 129 background, Ter causes tumor development in addition to sterility. Therefore, Ter acts as a modifier of 129-derived TGCT susceptibility genes. Ter was identified to be a mutation that inactivates the Dead-end1 (Dnd1) gene. In this perspective, I discuss the possible areas of future investigations to elucidate the mechanism of TGCT development
due to Dnd1 inactivation.
Received 29 September 2006; received after revision 29 January 2007; accepted 19 February 2007 相似文献
14.
Ca2+ signaling plays a crucial role in virtually all cellular processes, from the origin of new life at fertilization to the end
of life when cells die. Both the influx of external Ca2+ through Ca2+-permeable channels and its release from intracellular stores are essential to the signaling function. Intracellular Ca2+ is influenced by mitogenic factors which control the entry and progression of the cell cycle; this is a strong indication
for a role of Ca2+ in the control of the cycle, but surprisingly, the possibility of such a role has only been paid scant attention in the literature.
Substantial progress has nevertheless been made in recent years in relating Ca2+ and the principal decoder of its information, calmodulin, to the modulation of various cycle steps. The aim of this review
is to critically discuss the evidence for a role of Ca2+ in the cell cycle and to discuss Ca2+-dependent pathways regulating cell growth and differentiation.
Received 2 March 2005; received after revision 9 May 2005; accepted 24 May 2005 相似文献
15.
Hu QD Lu H Huo K Ying K Li J Xie Y Mao Y Li YY 《Cellular and molecular life sciences : CMLS》2003,60(8):1725-1732
The Saccharomyces cerevisiae TPT1 gene plays a role in removing the 2-phosphate from ligated tRNA during the maturation of pre-tRNA. Here we reported the cloning and characterization of the human TRPT1 gene as a homolog of yeast TPT1. The TRPT1 gene is located at human chromosome 11q13 and encodes a polypeptide of 253 amino acids. BLAST searches with its amino acid sequence revealed the ubiquitous occurrence of TRPT1 homologs and their functional relationships with the presence of the DUF60/KptA domain. Northern analysis demonstrated that the gene is primarily expressed in heart and skeletal muscle, with lower or undetectable levels in other tissues studied. A plasmid-shuffling experiment showed that the human TRPT1 gene could complement the tpt1 mutation in S. cerevisiaeReceived 19 March 2003; received after revision 25 April 2003; accepted 22 May 2003 相似文献
16.
Expression and immunolocalisation of odorant-binding and chemosensory proteins in locusts 总被引:7,自引:0,他引:7
Jin X Brandazza A Navarrini A Ban L Zhang S Steinbrecht RA Zhang L Pelosi P 《Cellular and molecular life sciences : CMLS》2005,62(10):1156-1166
We have identified, cloned and expressed a new chemosensory protein (CSP) in the desert locust Schistocerca gregaria belonging to a third sub-class of these polypeptides. Polyclonal antibodies stained a band of 14 kDa, as expected, in the extracts of antennae and palps of the adults, but not in the 4th and 5th instars. In the related species Locusta migratoria, instead, the same antibodies cross-reacted only with a band of apparent molecular mass of 35 kDa in the extract of 1st–5th instars, but not in the adults. The recombinant protein binds the fluorescent probe N-phenyl-1-naphthylamine, but none of the compounds so far reported as pheromones for S. gregaria. The expression of the odorant-binding protein (OBP) and of CSPs of sub-classes I and II was also monitored in antennae, tarsi, palpi, wings and other organs of solitary and gregarious locusts in their nymphal and adult stages. OBP was found to be antenna specific, where it is expressed at least from the 3rd instar in both solitary and gregarious locusts. CSPs, instead, appear to be more ubiquitous, with different expression patterns, according to the sub-class. Immunocytochemistry experiments revealed that OBP is present in the sensillum lymph of sensilla trichodea and basiconica, while CSP-I and CSP-III were found in the outer sensillum lymph of sensilla chaetica and in the sub-cuticular space between epidermis and cuticle of the antenna. Sensilla chaetica on other parts of the body showed the same expression of CSP-I as those on the antenna.Received 11 Janury 2005; received after revision 21 February 2005; accepted 18 March 2005X. Jin and A. Brandazza contributed equally to this work. 相似文献
17.
Dolezel D Zdechovanova L Sauman I Hodkova M 《Cellular and molecular life sciences : CMLS》2008,65(6):964-969
Current models state that insect peripheral oscillators are directly responsive to light, while mammalian peripheral clock
genes are coordinated by a master clock in the brain via intermediate factors, possibly hormonal. We show that the expression
levels of two circadian clock genes, period (per) and Par Domain Protein 1 (Pdp1) in the peripheral tissue of an insect model species, the linden bug Pyrrhocoris apterus, are inversely affected by contrasting photoperiods. The effect of photoperiod on per and Pdp1 mRNA levels was found to be mediated by the corpus allatum, an endocrine gland producing juvenile hormone. Our results
provide the first experimental evidence for the effect of an endocrine gland on circadian clock gene expression in insects.
Received 31 October 2007; received after revision 7 January 2008; accepted 9 January 2008
D. Dolezel, L. Zdechovanova: These authors contributed equally to this work. 相似文献
18.
Koleva M Kappler R Vogler M Herwig A Fulda S Hahn H 《Cellular and molecular life sciences : CMLS》2005,62(16):1863-1870
Muscle satellite cells are believed to form a stable, self-renewing pool of stem cells in adult muscle where they function in tissue growth and repair. A regulatory disruption of growth and differentiation of these cells is assumed to result in tumor formation. Here we provide for the first time evidence that sonic hedgehog (Shh) regulates the cell fate of adult muscle satellite cells in mammals. Shh promotes cell division of satellite cells (and of the related model C2C12 cells) and prevents their differentiation into multinucleated myotubes. In addition, Shh inhibits caspase-3 activation and apoptosis induced by serum deprivation. These effects of Shh are reversed by simultaneous administration of cyclopamine, a specific inhibitor of the Shh pathway. Taken together, Shh acts as a proliferation and survival factor of satellite cells in the adult muscle. Our results support the hypothesis of the rhabdomyosarcoma origin from satellite cells and suggest a role for Shh in this process.Received 23 February 2005; received after revision 2 May 2005; accepted 9 June 2005 相似文献
19.
The surfaces of mammalian cells are covered by a variety of carbohydrates linked to proteins
and lipids. N-glycans are commonly found carbohydrates in plasma
membrane proteins. The structure and biosynthetic pathway of
N-glycans have been analyzed extensively. However, functional
analysis of cell surface N-glycans is just under way with recent
studies of targeted disruption of genes involved in N-glycan
synthesis. This review briefly introduces the potential role of processing -mannosidases
in N-glycan biosynthesis and recent findings derived from the
-mannosidase IIx (MX) gene knockout mouse, which shows male infertility. Thus, the MX gene
knockout experiment unveiled a novel function of specific
N-glycan, which is
N-acetylglucosamine-terminated and fucosylated triantennary
structure, in the adhesion between germ cells and Sertoli cells. Analysis of the MX gene knockout
mouse is a good example of a multidisciplinary approach leading to a novel discovery in the
emerging field of glycobiology.Received 29 November 2002; received after revision 30 December 2002; accepted 20 January 2003 相似文献
20.
X. M. Jia Y. Wang Y. Jia P. H. Gao Y. G. Xu L. Wang Y. Y. Cao Y. B. Cao L. X. Zhang Y. Y. Jiang 《Cellular and molecular life sciences : CMLS》2009,66(1):122-134
The calcineurin pathway has been reported to be essential for the development of azole resistance in Candida albicans. The depletion or ectopic over-expression of RTA2 increased or decreased susceptibility of C. albicans to azoles, respectively. CaCl2- induced activation of the calcineurin pathway in wildtype C. albicans promoted resistance to azoles, while the Ca
2+ chelator (EGTA), calcineurin inhibitors (FK506 and cyclosporin A) and the deletion of RTA2 blocked the resistance-promoting effects of CaCl2. Furthermore, we found that RTA2 was up-regulated in a calcineurin-dependent manner. The depletion of RTA2 also made the cell membrane of C. albicans liable to be destroyed by azoles and RTA2 over-expression attenuated the destroying effects. Finally, the disruption of RTA2 caused an increased accumulation of dihydrosphingosine (DHS), one of the two sphingolipid long-chain bases, by decreasing
release of DHS. In conclusion, our findings suggest that RTA2 is involved in calcineurin-mediated azole resistance and sphingoid long-chain base release in C. albicans.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.
Received 14 July 2008; received after revision 29 August 2008; accepted 16 September 2008 相似文献