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48-602MAG
Buffer Detection Kit for Magnetic Beads
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Space Saver Option Customers purchasing multiple kits may choose to save storage space by eliminating the kit packaging and receiving their multiplex assay components in plastic bags for more compact storage.
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Anti-Brain Derived Neurotrophic Factor Antibody is an antibody against Brain Derived Neurotrophic Factor for use in ELISA, WB, IH.
Key Applications
ELISA
Western Blotting
Immunohistochemistry
Affects Function
Application Notes
Immunohistochemistry: 1:200-1:2,000 (see suggested protocol).
Immunoblotting: 1:200-1:2,000 we recommend preparing the BDNF samples for western blot by the method of Semba-Katoh, R et.al (J. Neurochemistry 69(1):34-42, 1997) because BDNF is not easily extracted in standard buffers. Dissected tissues should be homogenized in 10 volumes of 100mM phosphate buffer containing 1mM EDTA, 2M guanidine hydrochloride (pH 7.2), and three protease inhibitors, 10mM N-ethylmaleimide, 0.36mM pepstatin, and 1mM PMSF. Homogenates are then sonicated and centrifuged at 46K x g for 30 minutes at 4°C.
ELISA: 1:200-1:2,000
Inhibition of biological activity in vitro: 1:10-1:50
Use neat for in vivo animal studies.
Optimal working dilutions must be determined by end user.
Biological Information
Immunogen
Recombinant Human Brain Derived Neurotrophic Factor (BDNF).
Host
Sheep
Specificity
Brain Derived Neurotrophic Factor (BDNF). Neutralizes BDNF, but not other neurotrophins. By one site ELISA, less than 1% cross-reactivity against mouse NGF, recombinant human NT3 or neurotrophin 4.
The antibody was tested on human and rat derived samples, but based on sequence similarity it is expected to react with mouse and other mammalian species. The peptide sequences of human, rat and mouse BDNF are identical.
The protein encoded by this gene is a member of the nerve growth factor family. It is induced by cortical neurons, and is necessary for survival of striatal neurons in the brain. Expression of this gene is reduced in both Alzheimer's and Huntington disease patients. This gene may play a role in the regulation of stress response and in the biology of mood disorders. Multiple transcript variants encoding distinct isoforms have been described for this gene, but the full-length nature of only some could be determined.
FUNCTION: SwissProt: P23560 # Promotes the survival of neuronal populations that are all located either in the central nervous system or directly connected to it. Major regulator of synaptic transmission and plasticity at adult synapses in many regions of the CNS. The versatility of BDNF is emphasized by its contribution to a range of adaptive neuronal responses including long-term potentiation (LTP), long-term depression (LTD), certain forms of short-term synaptic plasticity, as well as homeostatic regulation of intrinsic neuronal excitability. SIZE: 247 amino acids; 27818 Da SUBUNIT: Monomers and homodimers. Binds to NTRK2/TRKB. SUBCELLULAR LOCATION: Secreted. PTM: The propeptide is N-glycosylated and glycosulfated. & Converted into mature BDNF by plasmin (PLG) (By similarity). DISEASE: SwissProt: P23560 # Defects in BDNF are a cause of congenital central hypoventilation syndrome (CCHS) [MIM:209880]; also known as congenital failure of autonomic control or Ondine curse. CCHS is a rare disorder characterized by abnormal control of respiration in the absence of neuromuscular or lung disease, or an identifiable brain stem lesion. A deficiency in autonomic control of respiration results in inadequate or negligible ventilatory and arousal responses to hypercapnia and hypoxemia. CCHS is frequently complicated with neurocristopathies such as Hirschsprung disease that occurs in about 16% of CCHS cases. SIMILARITY: SwissProt: P23560 ## Belongs to the NGF-beta family.
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 lyophilized material at -20 to -70°C for up to 12 months after date of receipt. After reconstitution maintain at -20 to -70°C in undiluted aliquots for up to 6 months. Avoid repeated freeze/thaw cycles. Glycerol (ACS grade or better) can be added (1:1) for additional stability.
The X-linked transcriptional repressor methyl CpG binding protein 2 (MeCP2), known for its role in the neurodevelopmental disorder Rett syndrome, is emerging as an important regulator of neuroplasticity in postmitotic neurons. Cocaine addiction is commonly viewed as a disorder of neuroplasticity, but the potential involvement of MeCP2 has not been explored. Here we identify a key role for MeCP2 in the dorsal striatum in the escalating cocaine intake seen in rats with extended access to the drug, a process that mimics the increasingly uncontrolled cocaine use seen in addicted humans. MeCP2 regulates cocaine intake through homeostatic interactions with microRNA-212 (miR-212) to control the effects of cocaine on striatal brain-derived neurotrophic factor (BDNF) levels. These data suggest that homeostatic interactions between MeCP2 and miR-212 in dorsal striatum may be important in regulating vulnerability to cocaine addiction.
Nicotinic alpha 7 receptor clusters on hippocampal GABAergic neurons: regulation by synaptic activity and neurotrophins. Kawai, Hideki, et al. J. Neurosci., 22: 7903-12 (2002)
2002
Nicotinic acetylcholine receptors containing the alpha7 gene product are expressed at substantial levels in the hippocampus. Because of their specific locations and their high relative calcium permeability, the receptors not only mediate cholinergic transmission in the hippocampus but also influence signaling at noncholinergic synapses. We have used fluorescently labeled alpha-bungarotoxin to image alpha7-containing receptors on hippocampal neurons and to examine their regulation in culture. The highest levels of staining for such receptors were most commonly found on GABAergic interneurons identified immunohistochemically. The receptors were distributed in clusters on the soma and dendrites and were localized in part at GABAergic synapses. A 3 d blockade of electrical activity with tetrodotoxin or NMDA receptors with APV dramatically reduced the proportion of GABAergic neurons expressing high levels of receptor staining and reduced the mean number of distinguishable receptor clusters on individual neurons. Blockade of either GABA(A) receptors with bicuculline or nicotinic receptors with d-tubocurarine had no effect, although exposure to nicotine could increase the level of receptor staining. Anti-BDNF and anti-NGF antibodies produced decrements equivalent to those of tetrodotoxin and APV, whereas addition of BDNF and NGF each increased staining levels and increased the number of distinguishable receptor clusters on GABAergic neurons. The exogenous neurotrophins could not, however, overcome the effects of either tetrodotoxin or APV. The results indicate that both NMDA receptor activation and the neurotrophins BDNF and NGF are necessary to sustain the distribution patterns of alpha7-containing nicotinic receptors on GABAergic hippocampal neurons.
