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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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Gewähltes Kit
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96-Well Plate
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Weitere Reagenzien hinzufügen (MAPmates erfordern die Verwendung eines Puffer- und Detektionskits)
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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
Platzsparende Option Kunden, die mehrere Kits kaufen, können ihre Multiplex-Assaykomponenten in Kunststoffbeuteln anstelle von Packungen erhalten, um eine kompaktere Lagerung zu ermöglichen.
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Anti-Caspase 9 Antibody, clone 2-23 is an antibody against Caspase 9 for use in IP, WB, IH(P).
Key Applications
Immunoprecipitation
Western Blotting
Immunohistochemistry (Paraffin)
Application Notes
Western blot: 1:1000 Immunohistochemistry (frozen and paraffin): 1:500 - 1:1000
Optimal working dilutions must be determined by end user.
Biological Information
Immunogen
Recombinant human caspase-9 prodomain
Clone
2-23
Concentration
Please refer to the Certificate of Analysis for the lot-specific concentration.
Host
Mouse
Specificity
Recognizes 46-48 kDa full-length procaspase-9, human recombinant caspase-9 and procaspase-9 from human cell lysates. Highly specific to caspase-9 and shows no cross-reaction with other caspase family members. Activation of procaspase-9 by Apaf-1 in the cytochrome c pathway requires proteolytic cleavage to generate active caspase-9. Once activated, capsase-9 initiates a caspase cascade involving the downstream executioner caspases 3, 6 and 7.
This gene encodes a member of the cysteine-aspartic acid protease (caspase) family. Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. Caspases exist as inactive proenzymes which undergo proteolytic processing at conserved aspartic residues to produce two subunits, large and small, that dimerize to form the active enzyme. This protein is processed by caspase APAF1; this step is thought to be one of the earliest in the caspase activation cascade. Alternative splicing results in two transcript variants which encode different isoforms.
FUNCTION: SwissProt: P55211 # Isoform 2 lacks activity is an dominant-negative inhibitor of caspase-9. SIZE: 416 amino acids; 46281 Da SUBUNIT: Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 35 kDa (p35) and a 10 kDa (p10) subunit. Caspase-9 and APAF1 bind to each other via their respective NH2-terminal CED-3 homologous domains in the presence of cytochrome C and ATP. Interacts with the inhibitors BIRC2, BIRC4, BIRC5 and BIRC7. TISSUE SPECIFICITY: Ubiquitous, with highest expression in the heart, moderate expression in liver, skeletal muscle, and pancreas. Low levels in all other tissues. PTM: Cleavages at Asp-315 by granzyme B and at Asp-330 by caspase- 3 generate the two active subunits. Caspase-8 and -10 can also be involved in these processing events. SIMILARITY: SwissProt: P55211 ## Belongs to the peptidase C14 family. & Contains 1 CARD domain.
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Usage Statement
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.
Storage and Shipping Information
Storage Conditions
Maintain refrigerated at 2-8°C in undiluted aliquots for up to 12 months.
Uncoupling oxidative/energy metabolism with low sub chronic doses of 3-nitropropionic acid or iodoacetate in vivo produces striatal cell damage. Rodríguez, E; Rivera, I; Astorga, S; Mendoza, E; García, F; Hernández-Echeagaray, E International journal of biological sciences
6
199-212
2009
A variety of evidence suggests that the failure of cellular metabolism is one of the underlying causes of neurodegenerative diseases. For example, the inhibition of mitochondrial function produces a pattern of cellular pathology in the striatum that resembles that seen in Huntington's disease. However, neurons can also generate ATP through the glycolytic pathway. Recent work has suggested a direct interaction between mutated huntingtin and a key enzyme in the glycolytic pathway, glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Yet little work has been gone into examination of the cellular pathology that results from the inhibition of this alternative energy source. Therefore, the aim of the present study is to characterize the cellular pathology that results in the striatum of mice after treatment with a toxin (iodoacete, IOA) that compromises anaerobic metabolism. This striatal pathology is compared to that produced by a widely studied blocker of mitochondrial function (3-nitropropionic acid, 3-NP). We found that low doses of either toxin resulted in significant pathology in the mouse striatum. Signs of apoptosis were observed in both experimental groups, although apoptosis triggered by IOA treatment was independent from caspase-3 activation. Importantly, each toxin appears to produce cellular damage through distinct mechanisms; only 3-NP generated clear evidence of oxidative stress as well as inhibition of endogenous antioxidants. Understanding the distinct pathological fingerprints of cell loss produced by blockade of oxidative and anaerobic metabolisms may give us insights into neurodegenerative diseases.
Millipore’s Caspase Antibodies, proteins, and assays have been well validated and published. See below for a comprehensive list of our Caspase products, based on the expertise of Upstate & Chemicon. Weitere Informationen >>
