Rabbit antibody to proBDNF (69-82): whole serum

$190.00USD

Catalogue No.:	R-087-100
Batch No.:	See product label
Unit size:	100 µl
Antigen:	A synthetic peptide (C-ELLDEDQKVRPNEE) as a part of human BDNF precursor protein (aa: 69-82) conjugated to KLH has been used as the immunogen.
Other Names:	Brain-derived neurotrophic factor (Precursor); Abrineurin
Accession:	BDNF_HUMAN
Description:	BDNF belongs to the neurotrophin family and regulates the survival and differentiation of neurons during development. The alterations in BDNF expression induced by various kinds of brain insult including stress, ischemia, seizure activity and hypoglycemia, may contribute to some pathologies such as depression, epilepsy, Alzheimer's, and Parkinson's disease. FUNCTION: 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. SUBUNIT: Monomers and homodimers. Binds to NTRK2/TRKB. SUBCELLULAR LOCATION: Secreted protein. Post Translation Modification (PTM): The propeptide is N-glycosylated and glycosulfated. PTM: Converted into mature BDNF by plasmin (PLG) (By similarity). DISEASE: Defects in BDNF are a cause of congenital central hypoventilation syndrome (CCHS); 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: Belongs to the NGF-beta family.
Produced in:	NZ white rabbit
Purity:	Whole serum
Applications:	IHC, WB. A dilution of 1:1000 to 1:5000 is recommended for both applications. The optimal working dilution should be determined by the end user.
Specificity:	Used in western blot, this antiserum detects a 35 kDa band corresponding to the molecular weight of proBDNF. No cross reactivity with other proneurotrophins was detected.
Cross-react:	This antiserum is known to react with human, mouse and rat proBDNF and also expected to recognise other mammalian proBDNF.
Blast it:	If you would like to use this product in another species other than those specified here, or to see the shared ID between the immunogen used here in different species and/or other molecules, simply copy the immunogen (from the Immunogen field) and paste it HERE and blast/format it. Note that, antisera raised against synthetic peptides are quite often very specific for that peptide ie, only one single amino acid difference may be enough to restrict the specificity to a particular molecule. Regardless, you can always contact us if you need assistance with this.
Form:	Lyophilised
Reconstitution:	Reconstitute in 100 µl of sterile water. Centrifuge to remove any insoluble material.
Storage:	After reconstitution keep aliquots at -20°C for a higher stability, and at 4°C with an appropriate antibacterial agent. Glycerol (1:) may be added for an additional stability. Avoid repetitive freeze/thaw cycles.
Expiry Date:	12 months after purchase
References:	1. A Acheson et al (1995) Nat. 74: 450-3 2. Q Yan et al (1994) J. Neurosci. 14(9): 5281-91 3. XF Zhou et al (1996) Neurosci. 74: 945-53 4. XF Zhou, et al (1998) Exp. Neurol. 149: 237-42 5. B Mellstrom et al (2004) Crit Rev Neurobiol 16, 43-9 6. I Tapia-Arancibia et al (2004) Front Neuroendocrinol 25, 77-107 7. S Pezet, et al (2002) Brain Res Brain Res Rev 40, 240-9 8. Barde Y. A. et al (1989) EMBO J. 1: 549 9. Conner J et al. (1997) J. Neurosci. 17: 2295
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