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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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Kits für die zelluläre Signaltransduktion & MAPmates™
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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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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
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AB3598
Sigma-AldrichAnti-Mitochondria Antibody
Anti-Mitochondria Antibody is an antibody against Mitochondria for use in WB & IC.
More>>Anti-Mitochondria Antibody is an antibody against Mitochondria for use in WB & IC. Less<<
Anti-Mitochondria Antibody: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
Presenilin 1 is a protein found in brain cells. Presenilin 1 has a major influence on the risk of contracting alzheimer's disease. Its function is unknown. However, it may be involved in protein production and trafficking, especially during early development. More than 40 different mutations have been found in the presenilin 1 gene, and these mutations associate with early-onset familial alzheimer's disease. Mutations in presenilin 1 tend to elevate levels of amyloid beta in the blood, cerebrospinal fluid, and brains of those affected by mutations
References
Product Information
Format
Serum
HS Code
3002 15 90
Control
HeLa whole cell extract, human neuroblastoma SH-SY5Y cells
Anti-Mitochondria Antibody is an antibody against Mitochondria for use in WB & IC.
Key Applications
Western Blotting
Immunocytochemistry
Application Notes
Immunoblotting: 1:500-1:1000
Immunocytochemistry: 1:100-1:300 on COS7, HeLa, 293 and SK-N-MC cell lines.
Optimal working dilutions must be determined by the end user.
Biological Information
Immunogen
Presenilin 1 peptide conjugated to KLH.
Host
Rabbit
Specificity
Mitochondria. Recognizes a 62 kD protein of immunoblots of subcellular fractions enriched in mitochondrial fractions.
The antibody shows a moderate titer by ELISA to the immunogen peptide but does not immunoblot any expected presenilin 1 bands. Immunocytochemistry with the serum revealed a mitochondria-like staining that was still present after exhaustive preabsorption with the peptide. The staining co-localizes with CHEMICON's anti-mitochondria antibody MAB1273.
Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1; PSEN2) or in the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (main component of amyloid deposits found in AD brains). Presenilins are postulated to regulate APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is thought that the presenilins are involved in the cleavage of the Notch receptor, such that they either directly regulate gamma-secretase activity or themselves are protease enzymes. Multiple alternatively spliced transcript variants have been identified for this gene, the full-length natures of only some have been determined.
FUNCTION: SwissProt: P49768 # Probable catalytic subunit of the gamma-secretase complex, an endoprotease complex that catalyzes the intramembrane cleavage of integral membrane proteins such as Notch receptors and APP (beta-amyloid precursor protein). Requires the other members of the gamma-secretase complex to have a protease activity. May play a role in intracellular signaling and gene expression or in linking chromatin to the nuclear membrane. Stimulates cell-cell adhesion though its association with the E-cadherin/catenin complex. Under conditions of apoptosis or calcium influx, cleaves E-cadherin promoting the disassembly of the E-cadherin/catenin complex and increasing the pool of cytoplasmic beta-catenin, thus negatively regulating Wnt signaling. May also play a role in hematopoiesis. SIZE: 467 amino acids; 52668 Da SUBUNIT: Homodimer. Component of the gamma-secretase complex, a complex composed of a presenilin homodimer (PSEN1 or PSEN2), nicastrin (NCSTN), APH1 (APH1A or APH1B) and PEN2. Such minimal complex is sufficient for secretase activity. Other components which are associated with the complex include SLC25A64, SLC5A7, PHB and PSEN1 isoform 3. Predominantly heterodimer of a N-terminal (NTF) and a C-terminal (CTF) endoproteolytical fragment. Associates with proteolytic processed C-terminal fragments C83 and C99 of the amyloid precursor protein (APP). Associates with NOTCH1. Component of cadherin/catenin adhesion complexes through direct binding to CDH1 or CDH2. Interaction with CDH1 stabilizes the complex and stimulates cell-cell aggregation. Interaction with CDH2 is essential for trafficking of CDH2 from the endoplasmic reticulum to the plasma membrane. Interacts with CTNND2, CTNNB1, HERPUD1, FLNA, FLNB, MTCH1, PKP4 and PARL. Interacts through its N-terminus with isoform 3 of GFAP. Interacts with DOCK3 (By similarity). SUBCELLULAR LOCATION: Endoplasmic reticulum membrane; Multi-pass membrane protein. Golgi apparatus membrane; Multi-pass membrane protein. Cell surface. Note=Bound to NOTCH1 also at the cell surface. Colocalizes with CDH1/2 at sites of cell-cell contact. Colocalizes with CTNNB1 in the endoplasmic reticulum and the proximity of the plasma membrane. Also present in azurophil granules of neutrophils. TISSUE SPECIFICITY: Expressed in a wide range of tissues including various regions of the brain, liver, spleen and lymph nodes. DOMAIN: SwissProt: P49768 The PAL motif is required for normal active site conformation. PTM: Heterogeneous proteolytic processing generates N-terminal (NTF) and C-terminal (CTF) fragments of approximately 35 and 20 kDa, respectively. During apoptosis, the C-terminal fragment (CTF) is further cleaved by caspase-3 to produce the fragment, PS1- CTF12. & After endoproteolysis, the C-terminal fragment (CTF) is phosphorylated on serine residues by PKA and/or PKC. Phosphorylation on Ser-346 inhibits endoproteolysis. DISEASE: SwissProt: P49768 # Defects in PSEN1 are a cause of familial early-onset Alzheimer disease type 3 (AD3) [MIM:607822]. AD3 is the most severe form of the disease, with complete penetrance and an onset occurring as early as 30 years of age. The second form is late- onset AD (LOAD), with mean age of onset greater than 58 years. AD is an autosomal dominant neurodegenerative disorder characterized by progressive dementia, parkinsonism, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major protein found within these deposits is a small, insoluble and highly aggregating polypeptide, beta-amyloid protein (beta- APP42). Defects in PSEN1 result in an overproduction of beta- APP42. Variant Pro-166, a very aggressive mutation that causes onset of AD3 in adolescence, not only induces an exceptionally high increase of beta-APP42 production, but also impairs Notch intracellular domain production and Notch signaling, as well as beta-APP intracellular domain generation. & Defects in PSEN1 are a cause of frontotemporal dementia [MIM:600274]. SIMILARITY: Belongs to the peptidase A22A family.
Stem Cell Type
Neural Stem Cells
Molecular Weight
62 kDa
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 at -20°C in undiluted aliquots for up to 12 months. Avoid repeated freeze-thaw cycles.
Histone deacetylase (HDAC) inhibitors are promising candidates for molecular-targeted therapy for leukemia. In this study, we investigated the mechanisms of cytotoxic effects of depsipeptide (FK228), one of the most effective HDAC inhibitors against leukemia, using human myeloid leukemic cell lines HL-60 and K562. We found that FK228 activated caspase-9 and a subsequent caspase cascade by perturbing the mitochondrial membrane to release cytochrome c, which was almost completely blocked by overexpression of Bcl-2. The mitochondrial damage was caused by the translocation of Bax but not other pro-apoptotic Bcl-2 family proteins to the mitochondria. FK228 did not affect the interaction between Bax and Bax adaptor proteins such as 14-3-3theta and Ku70. FK228-induced apoptosis and mitochondrial translocation of Bax were markedly enhanced by the proteasome inhibitor bortezomib. The synergistic action of FK228 and bortezomib was at least partly mediated through conformational changes in Bax, which facilitate its translocation to the mitochondria. These results suggest that the combination of HDAC inhibitors and proteasome inhibitors is useful in the treatment of leukemia especially in the context of molecular-targeted therapy. The status of Bcl-2 and Bax may influence the sensitivity of tumors to this combination and thus can be a target of further therapeutic intervention.
Apaf-1 is a mediator of E2F-1-induced apoptosis. Furukawa, Y; Nishimura, N; Furukawa, Y; Satoh, M; Endo, H; Iwase, S; Yamada, H; Matsuda, M; Kano, Y; Nakamura, M The Journal of biological chemistry
277
39760-8
2002
E2F-1 is capable of promoting both cell cycle progression and apoptosis. The latter is important for suppressing untoward expansion of proliferating cells. In this study, we investigated its underlying mechanisms. E2F-1-induced apoptosis was accompanied by caspase-9 activation and inhibited by a specific inhibitor of caspase-9 in K562 sublines overexpressing E2F-1. E2F-1 enhanced the expression of Apaf-1 without the cytosolic accumulation of cytochrome c. Apaf-1-deficient melanoma cell lines were resistant to E2F-1, indicating that Apaf-1 is an essential element of E2F-1-mediated apoptosis. Finally, we isolated the promoter region of the Apaf-1 gene and found a putative binding site for E2F. A chromatin immunoprecipitation assay revealed that E2F-1 bound to Apaf-1 promoter upon E2F-1 overexpression, suggesting that Apaf-1 is under transcriptional regulation of E2F-1. These data demonstrate a novel mechanism of apoptosis in which an increase in Apaf-1 levels results in direct activation of caspase-9 without mitochondrial damage, leading to the initiation of a caspase cascade.
