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Wählen Sie konfigurierbare Panels & Premixed-Kits - ODER - Kits für die zelluläre Signaltransduktion & MAPmates™
Konfigurieren Sie Ihre MILLIPLEX® MAP-Kits und lassen sich den Preis anzeigen.
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Unser breites Angebot enthält Multiplex-Panels, für die Sie die Analyten auswählen können, die am besten für Ihre Anwendung geeignet sind. Unter einem separaten Register können Sie das Premixed-Cytokin-Format oder ein Singleplex-Kit wählen.
Kits für die zelluläre Signaltransduktion & MAPmates™
Wählen Sie gebrauchsfertige Kits zur Erforschung gesamter Signalwege oder Prozesse. Oder konfigurieren Sie Ihre eigenen Kits mit Singleplex MAPmates™.
Die folgenden MAPmates™ sollten nicht zusammen analysiert werden: -MAPmates™, die einen unterschiedlichen Assaypuffer erfordern. -Phosphospezifische und MAPmate™ Gesamtkombinationen wie Gesamt-GSK3β und Gesamt-GSK3β (Ser 9). -PanTyr und locusspezifische MAPmates™, z.B. Phospho-EGF-Rezeptor und Phospho-STAT1 (Tyr701). -Mehr als 1 Phospho-MAPmate™ für ein einziges Target (Akt, STAT3). -GAPDH und β-Tubulin können nicht mit Kits oder MAPmates™, die panTyr enthalten, analysiert werden.
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96-Well Plate
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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
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Detect Bcl-xL using this Anti-Bcl-xL Antibody, Phospho-specific validated for use in WB.
More>>Detect Bcl-xL using this Anti-Bcl-xL Antibody, Phospho-specific validated for use in WB. Less<<
Anti-Bcl-xL Antibody, Phospho-specific: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
Bcl-XL is one of the anti-apoptotic members of the Bcl-2 family of apoptosis regulators and is overexpressed in many human cancers. Studies by Dr. Haldar and his associates suggest that microtubule damaging drugs like Taxol or 2-methoxyestradiol induce phosphorylation of Bcl-XL at serine 62 by kinases such as Jun and this allows those cells to die by apoptosis.
The protein encoded by this gene belongs to the BCL-2 protein family. BCL-2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. The proteins encoded by this gene are located at the outer mitochondrial membrane, and have been shown to regulate outer mitochondrial membrane channel (VDAC) opening. VDAC regulates mitochondrial membrane potential, and thus controls the production of reactive oxygen species and release of cytochrome C by mitochondria, both of which are the potent inducers of cell apoptosis. Two alternatively spliced transcript variants, which encode distinct isoforms, have been reported. The longer isoform acts as an apoptotic inhibitor and the shorter form acts as an apoptotic activator.
FUNCTION: SwissProt: Q07817 # Potent inhibitor of cell death. Isoform Bcl-X(L) anti- apoptotic activity is inhibited by association with SIVA isoform 1. Inhibits activation of caspases (By similarity). Appears to regulate cell death by blocking the voltage-dependent anion channnel (VDAC) by binding to it and preventing the release of the caspase activator, cytochrome c, from the mitochondrial membrane. The Bcl-X(S) isoform promotes apoptosis. SIZE: 233 amino acids; 26049 Da SUBUNIT: Bcl-X(L) forms homodimers, and heterodimers with BAX, BAK and BCL2. Heterodimerization with BAX does not seem to be required for anti-apoptotic activity. Also interacts with BAD and BBC3. Isoform Bcl-X(L) binds to Siva isoform 1. Interacts with BCL2L11 (By similarity). Interacts with BECN1 and PGAM5. SUBCELLULAR LOCATION: Mitochondrion membrane; Single-pass membrane protein (By similarity). Nucleus envelope; Single-pass membrane protein; Cytoplasmic side (By similarity). Note=Mitochondrial membranes and perinuclear envelope (By similarity). TISSUE SPECIFICITY: Bcl-X(S) is expressed at high levels in cells that undergo a high rate of turnover, such as developing lymphocytes. In contrast, Bcl-X(L) is found in tissues containing long-lived postmitotic cells, such as adult brain. DOMAIN: SwissProt: Q07817 The BH4 motif is required for anti-apoptotic activity. The BH1 and BH2 motifs are required for both heterodimerization with other Bcl-2 family members and for repression of cell death. PTM: Proteolytically cleaved by caspases during apoptosis. The cleaved protein, lacking the BH4 motif, has pro-apoptotic activity. SIMILARITY: Belongs to the Bcl-2 family.
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Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Maintain at -80°C for up to 12 months from date of receipt. Avoid repeated freeze/thaw cycles.
Hypoxia counteracts taxol-induced apoptosis in MDA-MB-231 breast cancer cells: role of autophagy and JNK activation. Notte, A; Ninane, N; Arnould, T; Michiels, C Cell death & disease
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e638
2013
Cancer cell resistance against chemotherapy is still a heavy burden to improve anticancer treatments. Autophagy activation and the development of hypoxic regions within the tumors are known to promote cancer cell resistance. Therefore, we sought to evaluate the role of autophagy and hypoxia on the taxol-induced apoptosis in MDA-MB-231 breast cancer cells. The results showed that taxol induced apoptosis after 16 h of incubation, and that hypoxia protected MDA-MB-231 cells from taxol-induced apoptosis. In parallel, taxol induced autophagy activation already after 2 h of incubation both under normoxia and hypoxia. Autophagy activation after taxol exposure was shown to be a protective mechanism against taxol-induced cell death both under normoxia and hypoxia. However, at longer incubation time, the autophagic process reached a saturation point under normoxia leading to cell death, whereas under hypoxia, autophagy flow still correctly took place allowing the cells to survive. Autophagy induction is induced after taxol exposure via mechanistic target of rapamycin (mTOR) inhibition, which is more important in cells exposed to hypoxia. Taxol also induced c-Jun N-terminal kinase (JNK) activation and phosphorylation of its substrates B-cell CLL/lymphoma 2 (Bcl2) and BCL2-like 1 (BclXL) under normoxia and hypoxia very early after taxol exposure. Bcl2 and BclXL phosphorylation was decreased more importantly under hypoxia after long incubation time. The role of JNK in autophagy and apoptosis induction was studied using siRNAs. The results showed that JNK activation promotes resistance against taxol-induced apoptosis under normoxia and hypoxia without being involved in induction of autophagy. In conclusion, the resistance against taxol-induced cell death observed under hypoxia can be explained by a more effective autophagic flow activated via the classical mTOR pathway and by a mechanism involving JNK, which could be dependent on Bcl2 and BclXL phosphorylation but independent of JNK-induced autophagy activation.
Identification of a novel Bcl-xL phosphorylation site regulating the sensitivity of taxol- or 2-methoxyestradiol-induced apoptosis Basu, A. and Haldar, S. FEBS Letters, 538:41-47 (2003)
2003
