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Wählen Sie konfigurierbare Panels & Premixed-Kits - ODER - 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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96-Well Plate
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48-602MAG
Buffer Detection Kit for Magnetic Beads
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The microtubule-associated protein 2 (MAP-2) is an abundant neuronal cytoskeletal protein that binds to tubulin, stabilizes microtubules (Herzog and Weber, 1978), and is an excellent marker for neurons. MAP-2 is essential for the development and maintenance of neuronal morphology (Matus, 1991). Three primary isoforms of MAP-2, the high molecular weight MAP2a and MAP2b, and the low molecular weight MAP2c (resulting from alternate splicing of the MAP2 gene), have been identified in neurours. (Chung et al., 1996). The low molecular weight isoform, MAP2c, is expressed in developing brain and is down-regulated during brain maturation, whereas the high molecular weight MAP2b is expressed in both developing and adult brain. The MAP2a appears only after brain maturation (Tucker, 1990). All these forms bind to microtubules through a domain near the carboxyl terminus that contains either three or four similar repeats of a 31-amino-acid motif (Lewis et al., 1988). MAP-2 together with MAP-4 and tau proteins belong to the family of thermostable proteins associated with microtubules.
References
Product Information
Format
AlexaFluor®488
Control
Rat E18 cortex cells
Presentation
Purified rabbit polyclonal conjugated to Alexa Fluor® 488 in PBS with 0.1% sodium azide and 15 mg/mL BSA.
FUNCTION: The exact function of MAP2 is unknown but MAPs may stabilize the microtubules against depolymerization. They also seem to have a stiffening effect on microtubules.
DEVELOPMENTAL STAGE: Isoform MAP2C is expressed during embryonic brain development and until postanatal day 10. Isoform MAP2B is expressed throughout brain development.
PTM: Phosphorylated upon DNA damage, probably by ATM or ATR, by similarity. MAP2A/c is phosphorylated.
The unconjugated parent antibody (Cat. No. AB2290) has an observed molecular weight at ~260 kDa.
Physicochemical Information
Dimensions
Materials Information
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Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Evaluated by Immunocytochemistry in rat E18 cortex cells.
Immunocytochemistry Analysis: A 1:100 dilution of this antibody detected MAP2 in rat E18 cortex cells.
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 protected from light in undiluted aliquots for up to 6 months from date of receipt.
Triggering receptor expressed on myeloid cells 2 (TREM2) deficiency attenuates phagocytic activities of microglia and exacerbates ischemic damage in experimental stroke. Kawabori, M; Kacimi, R; Kauppinen, T; Calosing, C; Kim, JY; Hsieh, CL; Nakamura, MC; Yenari, MA The Journal of neuroscience : the official journal of the Society for Neuroscience
35
3384-96
2015
Clearing cellular debris after brain injury represents an important mechanism in regaining tissue homeostasis and promoting functional recovery. Triggering receptor expressed on myeloid cells-2 (TREM2) is a newly identified receptor expressed on microglia and is thought to phagocytose damaged brain cells. The precise role of TREM2 during ischemic stroke has not been fully understood. We explore TREM2 in both in vitro and in vivo stroke models and identify a potential endogenous TREM2 ligand. TREM2 knockdown in microglia reduced microglial activation to an amoeboid phenotype and decreased the phagocytosis of injured neurons. Phagocytosis and infarcted brain tissue resorption was reduced in TREM2 knock-out (KO) mice compared with wild-type (WT) mice. TREM2 KO mice also had worsened neurological recovery and decreased viable brain tissue in the ipsilateral hemisphere. The numbers of activated microglia and phagocytes in TREM2 KO mice were decreased compared with WT mice, and foamy macrophages were nearly absent in the TREM2 KO mice. Postischemia, TREM2 was highly expressed on microglia and TREM2-Fc fusion protein (used as a probe to identify potential TREM2 binding partners) bound to an unknown TREM2 ligand that colocalized to neurons. Oxygen glucose deprivation-exposed neuronal media, or cellular fractions containing nuclei or purified DNA, but not cytosolic fractions, stimulated signaling through TREM2. TREM2-Fc fusion protein pulled down nucleic acids from ischemic brain lysate. These findings establish the relevance of TREM2 in the phagocytosis of the infarcted brain and emphasize its role in influencing neurological outcomes following stroke. Further, nucleic acids may be one potential ligand of TREM2 in brain ischemia.
