Therapie der Herzinsuffizienz

Krautwald, A; Krautwald, G. F.; Krautwald, E.

doi:10.1007/978-3-642-97060-3_28

Cited by 4 publications

(4 citation statements)

References 192 publications

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“…Cell Lysis and Immunoblotting-Cells were lysed in modified ice-cold Frackelton cell lysis buffer (18). Insoluble material was removed by centrifugation (14,000 ϫ g for 10 min at 4°C).…”

Section: Methodsmentioning

confidence: 99%

Transduction of the TAT-FLIP Fusion Protein Results in Transient Resistance to Fas-induced Apoptosis in Vivo

Krautwald¹,

Ziegler²,

Tiede³

et al. 2004

Journal of Biological Chemistry

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Although tightly regulated programmed cell death (apoptosis) possesses great importance for tissue homeostasis, several pathologic processes are associated with organ failure due to adversely activated cell apoptosis. Transient increase in apoptosis has been shown to cause organ damage during fulminant hepatitis B, autoimmune diseases, ischemia-reperfusion injury, sepsis, or allograft rejection. A defined and temporary inhibition of cell apoptosis may therefore be of high clinical relevance. Activation of death receptors results in caspase-8 recruitment to the death-inducing signaling complex, which initiates the apoptotic process through cleavage of caspase-8 and downstream substrates. This initial step may be inhibited by the caspase-8 inhibitor FLIP (FLICE inhibitory protein). To specifically inhibit the initiation of death receptor-mediated apoptosis we constructed a fusion protein containing FLIP fused N-terminally to the human immunodeficiency virus TAT domain. This TAT domain allows the fusion protein to cross the cell membrane and thus makes the Because of severe organ damage due to misregulated apoptosis in various diseases, intense studies have focused on apoptosis signaling pathways triggered by death receptors and their ligands including the Fas ligand, the tumor necrosis factor, and the tumor necrosis factor-related apoptosisinducing ligand (1-3). Fas (APO-1/CD95) surface expression does not necessarily render cells susceptible to Fas ligandinduced apoptosis because of counteracting physiological cellular inhibitors. One of these regulators of death receptormediated apoptosis was termed FLIP 1 (for FLICE inhibitory protein), which is predominantly expressed in lymphoid tissues (4, 5). Cross-linking of Fas-sensitive cells by the Fas ligand or an agonistic antibody induces apoptosis through procaspase-8 recruitment to the Fas-mediated death-inducing signaling complex (DISC), where procaspase-8 is cleaved to initiate apoptosis through a systematic cleavage of downstream substrates. The recruitment of the caspase-8 inhibitor cFLIP into the DISC prevents the cleavage of procaspase-8, resulting in concomitantly reduced apoptosis (6).Multiple splice variants of cFLIP have been reported, but to date only a long and a short form, designated cFLIP L and cFLIP S , respectively, could be detected on a protein level. It has been shown that, in the presence of cFLIP S , procaspase-8 is recruited into the DISC but remains unprocessed (7). Thus FLIP S appears to be a good candidate to block apoptosis in death receptor-mediated caspase-8 dependent pathways.In previous investigations it has been demonstrated that protein transduction is a powerful tool for introducing fulllength proteins into cells without the help of viral or chemical transporters (8,9). The principle of protein transduction originates from the biology of various viruses. In vivo analysis of the transduction properties of the HIV TAT domain demonstrated that almost all cells within the body, even those protected by the blood-brain barrier, were targ...

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“…Cell Lysis and Immunoblotting-Cells were lysed in modified ice-cold Frackelton cell lysis buffer (18). Insoluble material was removed by centrifugation (14,000 ϫ g for 10 min at 4°C).…”

Section: Methodsmentioning

confidence: 99%

Transduction of the TAT-FLIP Fusion Protein Results in Transient Resistance to Fas-induced Apoptosis in Vivo

Krautwald¹,

Ziegler²,

Tiede³

et al. 2004

Journal of Biological Chemistry

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“…Extensive reaction optimization and synthetic workarounds can be necessary to access the other diastereomers. 39 In the present case of setting two consecutive axes of chirality, when each axis is set by a different reaction (and thus differing reaction mechanisms), there exists a requirement for catalyst control, and any substrate-controlled selectivity biases must be identified and overcome.…”

Section: Resultsmentioning

confidence: 99%

Catalytic Dynamic Kinetic Resolutions in Tandem to Construct Two-Axis Terphenyl Atropisomers

et al. 2020

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The defined structure of molecules bearing multiple stereogenic axes is of increasing relevance to materials science, pharmaceuticals, and catalysis. However, catalytic enantioselective approaches to control multiple stereogenic axes remain synthetically challenging. We report the catalytic synthesis of two-axis terphenyl atropisomers, with complementary strategies to both chlorinated and brominated variants, formed with high diastereo-and enantioselectivity. The chemistry proceeds through a sequence of two distinct dynamic kinetic resolutions: first, an atroposelective ring-opening of Bringmann-type lactones produces a product with one established axis of chirality; second, a stereoselective arene halogenation delivers the product with the second axis of chirality established. In order to achieve these results, a class of Brønsted basic guanidinylated peptides, which catalyze an efficient atroposelective chlorination, is reported for the first time. In addition, a complementary bromination is reported, which also establishes the second stereogenic axis. These bromo-terphenyls are accessible following the discovery that chiral anion phase transfer catalysis by C 2 -symmetric phosphoric acids allows catalyst control in the second stereochemistry-determining event. Accordingly, we established the fully catalyst-controlled stereodivergent synthesis of all possible chlorinated stereoisomers, while also demonstrating diastereodivergence in the brominated variants, with significant levels of enantioselectivity in both cases.

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“…In contrast, monocytes and maturing macrophages secrete TNFα, IL-1β, IL-6 and IL-15 in response to IL-16 [41]. IL-16 treatment of macrophages has also been reported to result in the activation of the SAPK signaling pathway [42].…”

Section: Control Of Hiv-1 Ltr-mediated Transcription I Pro-inflammatmentioning

confidence: 96%

Modulation of HIV-1 Transcription by Cytokines and Chemokines

Copeland¹

2005

MRMC

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Infection with HIV results in the modulation of circulating levels of many host factors. Several host proteins that are up-regulated in HIV infection have the potential to influence virus replication. More specifically, the transcription of HIV-1 can be modulated in vivo by host proteins, including cytokines and chemokines. Cytokines modulate transcription mediated by the HIV-1 long terminal repeat (LTR) via multiple signal transduction pathways with resulting recruitment of numerous transcription factors, including NFkappaB, C/EBP, AP-1, TCF-1alpha, NF-IL-6 and ISGF-3. The effects on transcription may vary depending upon the cell type studied and upon the timing of the exposure of infected or transfected cells to cytokines. Furthermore, studies of cytokine mediated activation or inhibition of LTR mediated transcription may also be affected by the presence of the HIV-1 trans-activating protein, Tat, which has significant impact upon the redox state of the cell. This review will examine the complexities of the positive and negative control of HIV transcription by cytokines and chemokines.

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Therapie der Herzinsuffizienz

Cited by 4 publications

References 192 publications

Transduction of the TAT-FLIP Fusion Protein Results in Transient Resistance to Fas-induced Apoptosis in Vivo

Transduction of the TAT-FLIP Fusion Protein Results in Transient Resistance to Fas-induced Apoptosis in Vivo

Catalytic Dynamic Kinetic Resolutions in Tandem to Construct Two-Axis Terphenyl Atropisomers

Modulation of HIV-1 Transcription by Cytokines and Chemokines

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