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Trigger insert

Interaction with a lipid bilayer driven by a potential difference and by polar and/or hydrophobic forces between the amino acid side chains of the pardaxin tetramers and the polar membrane lipid head group triggers insertion from a "raft" like structure. [Pg.362]

FIGURE 10.31 The umbrella model of membrane chamiel protein insertion. Hydrophobic helices insert directly into the core of the membrane, with amphipathic helices arrayed on the surface like an open umbrella. A trigger signal (low pH or a voltage gradient) draws some of the amphipathic helices into and across the membrane, causing the pore to open. [Pg.316]

Figure 3. Difference mass spectrum of the [HO—Fe—CH3] insertion intermediate at photolysis wavelengths of 570 nm (a) and 350 nm (b). Simple Fe—C bond fission is observed at both wavelengths, but photolysis at 350 nm also triggers the half reaction to produce Fe+ + methanol (CH3OH). Figure 3. Difference mass spectrum of the [HO—Fe—CH3] insertion intermediate at photolysis wavelengths of 570 nm (a) and 350 nm (b). Simple Fe—C bond fission is observed at both wavelengths, but photolysis at 350 nm also triggers the half reaction to produce Fe+ + methanol (CH3OH).
In a similar way as described for the hydroformylation, the rhodium-catalyzed silaformylation can also be used in a domino process. The elementary step is the formation of an alkenyl-rhodium species by insertion of an alkyne into a Rh-Si bond (silylrhodation), which provides the trigger for a carbocyclization, followed by an insertion of CO. Thus, when Matsuda and coworkers [216] treated a solution of the 1,6-enyne 6/2-87 in benzene with the dimethylphenylsilane under CO pressure (36 kg cm"2) in the presence of catalytic amounts of Rh4(CO)12, the cyclopentane derivative 6/2-88 was obtained in 85 % yield. The procedure is not restricted to the formation of carbocycles rather, heterocycles can also be synthesized using 1,6-enynes as 6/2-89 and 6/2-90 with a heteroatom in the tether (Scheme 6/2.19). Interestingly, 6/2-91 did not lead to the domino product neither could 1,7-enynes be used as substrates, while the Thorpe-Ingold effect (geminal substitution) seems important in achieving good yields. [Pg.435]

Patients receiving statins should have a fasting panel 4 to 8 weeks after the initial dose or dose changes. Liver function tests should be obtained at baseline and periodically thereafter based on package insert information. Some experts believe that monitoring for hepatotoxicity and myopathy should be triggered by symptoms. [Pg.123]

Very recently, Murakami has published an Rh(i)-catalyzed cyclization of 1,6-enynes triggered by addition of arylboronic acids (Scheme 74).281 Initial carborhodation of the alkyne moiety is followed by insertion into the alkene moiety. /3-Alkoxy elimination provides the final product 289 in good yield and regenerates the catalyst species. [Pg.335]

Most of the responses which lead to cytochrome c release are triggered by activated proapoptotic members of the Bcl-2 family which are directed to mitochondria, where they insert into the outer membrane. What mediates the specific targeting of these proteins to mitochondria, hi a recent work, Lutter et al. (2000) investigated this question using the proapoptotic Bcl-2 member (tBid) as a tool. These authors estabhshed a hposome model for cytochrome c release and recreated the lipid constitution of mitochondrial outer... [Pg.7]

Figure 3. Possible mechanisms of actions of Bcl-2 members. Two prevailing models through which Bcl-2 membas trigger cytochrome c release have been suggested. In both models phospholipids in the bilayer stnicture either individually and/or collectively induce a conformational change in Bcl-2 members, allowing them to insert into the outer mitochondrial membrane. In model 1 proapoptotic proteins destabilize the outer mitochondrial membrane, oligomerize and form channels through which cytochrome c and other proteins of the intermembrane space can escape.BcI-2 proteins such as Bax or tBid act in concert with other proteins of the BcI-2 family to form channels. In model 2 Bcl-2 members such as Bax interact with residoit proteins in the outer membrane (OM) such as the voltage-dependent anion... Figure 3. Possible mechanisms of actions of Bcl-2 members. Two prevailing models through which Bcl-2 membas trigger cytochrome c release have been suggested. In both models phospholipids in the bilayer stnicture either individually and/or collectively induce a conformational change in Bcl-2 members, allowing them to insert into the outer mitochondrial membrane. In model 1 proapoptotic proteins destabilize the outer mitochondrial membrane, oligomerize and form channels through which cytochrome c and other proteins of the intermembrane space can escape.BcI-2 proteins such as Bax or tBid act in concert with other proteins of the BcI-2 family to form channels. In model 2 Bcl-2 members such as Bax interact with residoit proteins in the outer membrane (OM) such as the voltage-dependent anion...
Insert the pH probe into the KHP solution. When the pH meter is stable, press TRIGGER on the CBL unit. [Pg.42]

However, within a few months, two of the nine children developed a form of leukemia that had been triggered by the insertion of the payload gene too close to a gene that controlled the division of those cells. Uncontrolled increases in the number of white blood cells cause leukemia. The two children were treated with chemotherapy for the leukemia. One patient s leukemia returned and the child was then treated with a bone marrow transplant, but subsequently died. The same study reported that a third child showed evidence of uncontrolled growth of white blood cells. In addition, a U.S. researcher reported that a monkey treated with cells changed by a similar vector died of a white blood cell tumor. The FDA called a halt to human... [Pg.91]

Mercury (Il)-catalyzed insertion of a nitrile into the cyclobutane ring of p-pinene [129] is regio- and stereospecific. The strained C-C bond is ideally substituted such that complexation of the double bond with Hg2+ triggers its heterolysis to generate a relatively stable acceptor (C+). [Pg.114]

This study reports that retrovirus vector insertion into a proto-oncogene activates proto-oncogene expression, which may trigger malignancy. [Pg.91]

Low pH of endosome triggers extension of HA fusion peptides, which insert into endosomal membrane. [Pg.388]


See other pages where Trigger insert is mentioned: [Pg.463]    [Pg.316]    [Pg.200]    [Pg.180]    [Pg.180]    [Pg.353]    [Pg.309]    [Pg.75]    [Pg.537]    [Pg.260]    [Pg.259]    [Pg.230]    [Pg.103]    [Pg.192]    [Pg.216]    [Pg.484]    [Pg.285]    [Pg.318]    [Pg.228]    [Pg.59]    [Pg.48]    [Pg.43]    [Pg.246]    [Pg.156]    [Pg.103]    [Pg.304]    [Pg.58]    [Pg.315]    [Pg.754]    [Pg.920]    [Pg.491]    [Pg.338]    [Pg.319]    [Pg.54]    [Pg.203]    [Pg.339]    [Pg.85]    [Pg.354]   
See also in sourсe #XX -- [ Pg.28 , Pg.156 ]




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Insert trigger, with

Triggerable

Triggers

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