BDNF Antibody [A7P4] | Primary Antibodies

Application: Reactivity: Human, Mouse

Usage Information

Dilution
WB1:1000 IP1:50

Application
WB, IP

Reactivity
Human, Mouse

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
28 kDa 28 kDa (ProBDNF), 12-14 kDa (Mature)
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
BDNF Antibody [A7P4] detects endogenous levels of total BDNF protein.

Clone
A7P4

Synonym(s)
Abrineurin; ANON2; BDNF; BDNF precursor form; brain derived neurotrophic factor; Brain-derived neurotrophic factor; BULN2; MGC34632; neurotrophin; ProBDNF

Background
BDNF (brain‑derived neurotrophic factor) is a dimeric secreted neurotrophin of the NGF/NT‑3/NT‑4 family that regulates neuronal growth, differentiation, survival, and synaptic plasticity across development and adulthood, and also modulates energy balance, behavior, and stress responses through actions in hypothalamic and limbic circuits. The precursor proBDNF is synthesized as a pre‑pro‑protein that is cleaved to proBDNF and further processed to mature BDNF (mBDNF); proBDNF preferentially engages the p75 neurotrophin receptor (p75NTR) often in complex with sortilin, while mBDNF binds with high affinity to the tropomyosin‑related kinase B receptor (TrkB), and these ligand–receptor pairings drive largely opposing synaptic outcomes. TrkB activation requires mBDNF dimerization and receptor dimerization with trans‑autophosphorylation of intracellular tyrosine residues that recruit Shc, Shp2, and PLCγ, initiating three major cascades: Ras–Raf–MEK–ERK signaling that supports neuronal differentiation, neurite growth, and activity‑dependent gene expression; PI3K–Akt–mTOR signaling that promotes survival, growth, and protein synthesis; and PLCγ–IP₃–DAG–PKC signaling with Ca²⁺ mobilization that underlies rapid modulation of synaptic strength. These pathways converge on transcription factors such as CREB and MEF2 and on local translation machinery, enabling BDNF to increase dendritic spine density, regulate AMPA and NMDA receptor trafficking, and stabilize long‑term potentiation in hippocampus and cortex, while proBDNF–p75NTR signaling enhances JNK activation, promotes long‑term depression, spine retraction, and in some contexts apoptotic or pruning‑like responses, establishing a bidirectional control system in which the balance of proBDNF and mBDNF shapes synaptic plasticity polarity. BDNF and TrkB are widely expressed throughout central and peripheral nervous systems, with high levels in hippocampus, cortex, amygdala, striatum, and hypothalamus; BDNF functions as a neurotransmitter modulator at excitatory and inhibitory synapses, regulates neurogenesis in adult hippocampal niches, and supports maturation and maintenance of multiple neuronal subtypes, including dopaminergic, serotonergic, and sensory neurons, while also influencing pain circuitry and stress axis regulation. Activity‑dependent transcription of BDNF is driven by Ca²⁺ influx through NMDA receptors and voltage‑gated Ca²⁺ channels, activation of CaMKs, ERK, and CREB, and promoter‑specific regulatory factors such as CaRF, allowing synaptic activity to induce BDNF expression and feed back onto synapses to implement synapse‑to‑nucleus‑to‑synapse signaling loops that underlie learning and memory. Circulating and brain BDNF levels are altered in numerous neurological and psychiatric disorders, including Alzheimer’s and Huntington’s diseases, major depression, bipolar disorder, schizophrenia, and anxiety, and BDNF Val66Met and other polymorphisms affect activity‑dependent secretion and have been associated with cognitive and affective phenotypes, supporting BDNF as both a mechanistic factor and a potential biomarker in CNS disease. BDNF expression in hypothalamic and mesolimbic circuits involved in feeding and reward links it to body‑weight regulation and energy metabolism, where BDNF–TrkB signaling influences satiety, locomotor activity, and fat oxidation via AMPK/ACC modulation, consistent with its requirement for normal appetite and energy expenditure.

Background

BDNF (brain‑derived neurotrophic factor) is a dimeric secreted neurotrophin of the NGF/NT‑3/NT‑4 family that regulates neuronal growth, differentiation, survival, and synaptic plasticity across development and adulthood, and also modulates energy balance, behavior, and stress responses through actions in hypothalamic and limbic circuits. The precursor proBDNF is synthesized as a pre‑pro‑protein that is cleaved to proBDNF and further processed to mature BDNF (mBDNF); proBDNF preferentially engages the p75 neurotrophin receptor (p75NTR) often in complex with sortilin, while mBDNF binds with high affinity to the tropomyosin‑related kinase B receptor (TrkB), and these ligand–receptor pairings drive largely opposing synaptic outcomes. TrkB activation requires mBDNF dimerization and receptor dimerization with trans‑autophosphorylation of intracellular tyrosine residues that recruit Shc, Shp2, and PLCγ, initiating three major cascades: Ras–Raf–MEK–ERK signaling that supports neuronal differentiation, neurite growth, and activity‑dependent gene expression; PI3K–Akt–mTOR signaling that promotes survival, growth, and protein synthesis; and PLCγ–IP₃–DAG–PKC signaling with Ca²⁺ mobilization that underlies rapid modulation of synaptic strength. These pathways converge on transcription factors such as CREB and MEF2 and on local translation machinery, enabling BDNF to increase dendritic spine density, regulate AMPA and NMDA receptor trafficking, and stabilize long‑term potentiation in hippocampus and cortex, while proBDNF–p75NTR signaling enhances JNK activation, promotes long‑term depression, spine retraction, and in some contexts apoptotic or pruning‑like responses, establishing a bidirectional control system in which the balance of proBDNF and mBDNF shapes synaptic plasticity polarity. BDNF and TrkB are widely expressed throughout central and peripheral nervous systems, with high levels in hippocampus, cortex, amygdala, striatum, and hypothalamus; BDNF functions as a neurotransmitter modulator at excitatory and inhibitory synapses, regulates neurogenesis in adult hippocampal niches, and supports maturation and maintenance of multiple neuronal subtypes, including dopaminergic, serotonergic, and sensory neurons, while also influencing pain circuitry and stress axis regulation. Activity‑dependent transcription of BDNF is driven by Ca²⁺ influx through NMDA receptors and voltage‑gated Ca²⁺ channels, activation of CaMKs, ERK, and CREB, and promoter‑specific regulatory factors such as CaRF, allowing synaptic activity to induce BDNF expression and feed back onto synapses to implement synapse‑to‑nucleus‑to‑synapse signaling loops that underlie learning and memory. Circulating and brain BDNF levels are altered in numerous neurological and psychiatric disorders, including Alzheimer’s and Huntington’s diseases, major depression, bipolar disorder, schizophrenia, and anxiety, and BDNF Val66Met and other polymorphisms affect activity‑dependent secretion and have been associated with cognitive and affective phenotypes, supporting BDNF as both a mechanistic factor and a potential biomarker in CNS disease. BDNF expression in hypothalamic and mesolimbic circuits involved in feeding and reward links it to body‑weight regulation and energy metabolism, where BDNF–TrkB signaling influences satiety, locomotor activity, and fat oxidation via AMPK/ACC modulation, consistent with its requirement for normal appetite and energy expenditure.

References
https://pubmed.ncbi.nlm.nih.gov/34071978/ https://pubmed.ncbi.nlm.nih.gov/33096634/

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%