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111.
Testing the covarion hypothesis of molecular evolution 总被引:14,自引:8,他引:6
The covarion hypothesis of molecular evolution states that the fixation of
mutations may alter the probability that any given position will fix the
next change. Tests of this hypothesis using the divergence of real
sequences are compromised because models of rate variation among sites
(e.g., the gamma version of the one-parameter equation) predict sequence
divergence values similar to those for the covarion process. This study
therefore focuses on the extent to which the varied and unvaried codons of
two well-diverged taxa are the same, because fewer are expected by the
covarion hypothesis than by the gamma model. The data for these tests are
the protein sequences of Cu, Zn superoxide dismutase (SOD) for mammals and
plants. Simulation analyses show that the covarion hypothesis makes better
predictions about the frequencies of varied and unhit positions in common
between these two taxa than does the gamma version of the one-parameter
model. Furthermore, the analysis of SOD tertiary structure demonstrates
that mammal and plant variabilities are distributed differently on the
protein. These results support the conclusions that the variable and
invariable codons of mammal and plant SODs are different and that the
covarion model explains the evolution of this protein better than the gamma
version of the one-parameter process. Unlike other models, the covarion
hypothesis accounts for rate fluctuations among positions over time, which
is an important parameter of molecular evolution.
相似文献
112.
Sterigmatocystin (STG) is a toxic metabolite produced by severalAspergillus species. Because of its toxic and carcinogenic properties the occurrence of STG in food is considered to represent a potential
hazard to man. The present study was designed to investigate following points:
相似文献
1 | A survey of STG incidence in Ras cheese on local markets. Ras cheese samples were collected from Cairo, Giza and Kalubia governorates. Thirty five percent of the samples contained the toxin with a mean value of 22.23 μg /kg |
2 | Fate of STG contaminating milk during Ras cheese processing. Milk was artificially contaminated with 125 μg/kg and processed into Ras cheese. Eighty percent of the toxin was distributed into the curd and 20% into the whey. Cheese ripening effected toxin content and the effect was temperature dependent. At 6°C: toxin concentration was slightly affected; at 20°C the toxin was reduced by 16% after 90 days when low toxin concentration was used. |
3 | Formation of STG byA versicolor mold on Ras cheese. Ras cheese blocks were contaminated with spores of the mold. Toxin production started after 45 days of ripening and reached a maximum at 90 days and then declined. Cow’s milk favoured toxin production over buffaloe’s. Aged cheese inhibited toxin production. |
113.
The class C L-type calcium (Ca(2+)) channels have been implicated in many important physiological processes. Here, we have identified a mouse vacuolar H(+)-ATPase (V-ATPase) G2 subunit protein that bound to the C-terminal domain of the pore-forming alpha(1C) subunit using a yeast two-hybrid screen. Protein-protein interaction between the V-ATPase G subunit and the alpha(1C) subunit was confirmed using in vitro GST pull-down assays and coimmunoprecipitation from intact cells. Moreover, treatment of cells expressing L-type Ca(2+) channels with a specific inhibitor of the V-ATPase blocked proper targeting of the channels to the plasma membrane. 相似文献
114.
Gerhardstein BL Gao T Bünemann M Puri TS Adair A Ma H Hosey MM 《The Journal of biological chemistry》2000,275(12):8556-8563
Although most L-type calcium channel alpha(1C) subunits isolated from heart or brain are approximately 190-kDa proteins that lack approximately 50 kDa of the C terminus, the C-terminal domain is present in intact cells. To test the hypothesis that the C terminus is processed but remains functionally associated with the channels, expressed, full-length alpha(1C) subunits were cleaved in vitro by chymotrypsin to generate a 190-kDa C-terminal truncated protein and C-terminal fragments of 30-56 kDa. These hydrophilic C-terminal fragments remained membrane-associated. A C-terminal proline-rich domain (PRD) was identified as the mediator of membrane association. The alpha(1C) PRD bound to SH3 domains in Src, Lyn, Hck, and the channel beta(2) subunit. Mutant alpha(1C) subunits lacking either approximately 50 kDa of the C terminus or the PRD produced increased barium currents through the channels, demonstrating that these domains participate in the previously described (Wei, X., Neely, a., Lacerda, A. E. Olcese, r., Stefani, E., Perez-Reyes, E., and Birnbaumer, L. (1994) J. Biol. Chem. 269, 1635-1640) inhibition of channel function by the C terminus. 相似文献
115.
Hosey MM Pals-Rylaarsdam R Lee KB Roseberry AG Benovic JL Gurevich VV Bünemann M 《Life sciences》1999,64(6-7):363-368
Multiple events are associated with the regulation of signaling by the M2 muscarinic cholinergic receptors (mAChRs). Desensitization of the attenuation of adenylyl cyclase by the M2 mAChRs appears to involve agonist-dependent phosphorylation of M2 mAChRs by G-protein coupled receptor kinases (GRKs) that phosphorylate the receptors in a serine/threonine rich motif in the 3rd intracellular domain of the receptors. Mutation of residues 307-311 from TVSTS to AVAAA in this domain of the human M2 mAChR results in a loss of receptor/G-protein uncoupling and a loss of arrestin binding. Agonist-induced sequestration of receptors away from their normal membrane environment is also regulated by agonist-induced phosphorylation of the M2 mAChRs on the 3rd intracellular domain, but in HEK cells, the predominant pathway of internalization is not regulated by GRKs or arrestins. This pathway of internalization is not inhibited by a dominant negative dynamin, and does not appear to involve either clathrin coated pits or caveolae. The signaling of the M2 mAChR to G-protein regulated inwardly rectifying K channels (GIRKs) can be modified by RGS proteins. In HEK cells, expression of RGS proteins leads to a constitutive activation of the channels through a mechanism that depends on Gbetagamma. RGS proteins appear to increase the concentration of free Gbetagamma in addition to acting as GAPs. Thus multiple mechanisms acting at either the level of the M2 mAChRs or the G-proteins can contribute to the regulation of signaling via the M2 mAChRs. 相似文献
116.
117.
118.
Annemarie MM Vlaar Tjerk de Nijs Marinus JPG van Kroonenburgh Werner H Mess Ania Winogrodzka Selma C Tromp Wim EJ Weber 《BMC neurology》2008,8(1):42
Background
Transcranial duplex sonography (TCD) of the substantia nigra has emerged as a promising, non-invasive tool to diagnose idiopathic Parkinson's disease (IPD). However, its diagnostic accuracy in patients with undefined parkinsonism remains to be determined. 相似文献119.
Exosomes secreted from mutant‐HIF‐1α‐modified bone‐marrow‐derived mesenchymal stem cells attenuate early steroid‐induced avascular necrosis of femoral head in rabbit
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120.
Voltage-dependent L-type calcium (Ca) channels are heteromultimeric proteins that are regulated through phosphorylation by cAMP-dependent protein kinase (PKA). We demonstrated that the beta 2 subunit was a substrate for PKA in intact cardiac myocytes through back-phosphorylation experiments. In addition, a heterologously expressed rat beta 2a subunit was phosphorylated at two sites in vitro by purified PKA. This beta 2a subunit contains two potential consensus sites for PKA-mediated phosphorylation at Thr164 and Ser591. However, upon mutation of both of these residues to alanines, the beta 2a subunit remained a good substrate for PKA. The actual sites of phosphorylation on the beta 2a subunit were identified by phosphopeptide mapping and microsequencing. Phosphopeptide maps of a bacterially expressed beta 2a subunit demonstrated that this subunit was phosphorylated similarly to the beta 2 subunit isolated from heart tissue and that the phosphorylation sites were contained in the unique C-terminal region. Microsequencing identified three serine residues, each of which conformed to loose consensus sites for PKA-mediated phosphorylation. Mutation of these residues to alanines resulted in the loss of the PKA-mediated phosphorylation of the beta 2a subunit. The results suggest that phosphorylation of the beta 2a subunit by PKA occurs at three loose consensus sites for PKA in the C-terminus and not at either of the two strong consensus sites for PKA. The results also highlight the danger of assuming that consensus sites represent actual sites of phosphorylation. The actual sites of PKA-mediated phosphorylation are conserved in most beta 2 subunit isoforms and thus represent potential sites for regulation of channel activity. The sites phosphorylated by PKA are not substrates for protein kinase C (PKC), as the mutated beta 2 subunits lacking PKA sites remained good substrates for PKC. 相似文献