BDNF Protein, Human (CHO)

BDNF Protein, Human (CHO) is a neurotrophin binding to the high-affinity tropomyosin-related receptor kinase B (TrkB) receptor to regulate neurodevelopmental processes, including neuronal survival, neuronal differentiation, and synaptic plasticity.

Recombinant Human BDNF/Brain-derived neurotrophic factor is a neurotrophin binding to the high-affinity tropomyosin-related receptor kinase B (TrkB) receptor to regulate neurodevelopmental processes, including neuronal survival, neuronal differentiation, and synaptic plasticity^[1]. Brain-derived neurotrophic factor (BDNF) is one of the most abundant neurotrophins in the mammalian central nervous system that promotes neuronal survival and differentiation. BDNF plays crucial roles in the cardiovascular system^[2].

The ED₅₀ is <4 μg/ml as measured by C6 cells. Immobilized Human BDNF at 5 μg/ml (100 μl/well) can bind NGF R, Human-Biotin with a linear range of 0.06-4 μg/ml.

Human

CHO

Tag Free

P23560 (H129-R247)

627  [NCBI]

HSDPARRGELSVCDSISEWVTAADKKTAVDMSGGTVTVLEKVPVSKGQLKQYFYETKCNPMGYTKEGCRGIDKRHWNSQCRTTQSYVRALTMDSKKRIGWRFIRIDTSCVCTLTIKRGR

12-14 kDa

Greater than 95% as determined by reducing SDS-PAGE.

Lyophilized powder

Lyophilized after extensive dialysis against PBS.

<0.2 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Li M, et al. Recombinant human brain-derived neurotrophic factor prevents neuronal apoptosis in a novel in vitro model of subarachnoid hemorrhage. Neuropsychiatr Dis Treat. 2017 Apr 3;13:1013-1021.  [Content Brief]

  [2]. Hang P, et al. Brain-derived neurotrophic factor attenuates doxorubicin-induced cardiac dysfunction through activating Akt signalling in rats. J Cell Mol Med. 2017 Apr;21(4):685-696.  [Content Brief]