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07-225

Sigma-Aldrich

Anti-TrkB Antibody

Upstate®, from rabbit

Synonym(s):

BDNF/NT-3 growth factors receptor, Neurotrophic tyrosine kinase receptor type 2, TrkB tyrosine kinase, neurotrophic tyrosine kinase receptor, type 2, tyrosine kinase receptor B

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

antibody form

purified antibody

antibody product type

primary antibodies

clone

polyclonal

species reactivity

mouse, rat

manufacturer/tradename

Upstate®

technique(s)

western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... NTRK2(4915)

General description

The Trk (tropomyosin-receptor-kinase) proto-oncogene family of receptor tyrosine kinases contains four members, TrkA, TrkB, TrkC, and TrkE, which are variably expressed throughout the central and peripheral nervous systems. TrkB is the high-affinity to the binding brain-derived neurotrophic factor (BDNF) receptor and neurotrophin-4/5 NT-4/5). TrkB is autophosphorylated on five cytoplasmic tyrosines. The binding of BDNF to TrkB receptor causes many intercellular cascades to be activated such as promoting survival of sensory neurons mainly through Shc site-independent pathways.The signaling activity of these receptors includes the Ras – MAP kinase pathway, and the PI3 Kinase pathway. These receptors are responsible for resistance to apoptosis, obesity, Alzheimer’s disease, and mood disorders.

Specificity

Recognizes TrkB, Mr 145 kDa, as well as an additional protein, Mr 90 kDa, which is likely a TrkB degradation product.

Immunogen

The entire extracellular domain (corresponding to residues 1–429) of the rat TrkB receptor, expressed in COS cells. The immunizing sequence has 97% identity with mouse TrkB and 88% identity with human TrkB.

Application

Research Category
Neuroscience
Research Sub Category
Neurochemistry & Neurotrophins
This Anti-TrkB Antibody is validated for use in WB for the detection of TrkB.

Quality

Evaluated by western blot on mouse brain membrane protein preparations.

Western Blot Analysis:
0.5-2 µg/mL of this antibody detected TrkB in mouse brain membrane protein preparations.

Target description

145 κDa

Physical form

Format: Purified
Protein A purified
Purified rabbit polyclonal in buffer containing 0.014 M phosphate buffer, pH 7.6, 0.175 M NaCl, 0.07% sodium azide, and 30% glycerol.

Storage and Stability

Stable for 1 year at -20ºC from date of receipt.

Analysis Note

Control
Brain tissue.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

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.

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Storage Class Code

10 - Combustible liquids

WGK

WGK 1


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Evidence that biological activity of NGF is mediated through a novel subclass of high affinity receptors
Weskamp, G and Reichardt, L F
Neuron, 6, 649-663 (1991)
JIP3 mediates TrkB axonal anterograde transport and enhances BDNF signaling by directly bridging TrkB with kinesin-1.
Huang, SH; Duan, S; Sun, T; Wang, J; Zhao, L; Geng, Z; Yan, J; Sun, HJ; Chen, ZY
The Journal of Neuroscience null
Zeeba D Kabir et al.
PloS one, 8(12), e84165-e84165 (2013-12-21)
Prenatal cocaine exposure has been shown to alter cognitive processes of exposed individuals, presumed to be a result of long-lasting molecular alterations in the brain. In adult prenatal cocaine exposed (PCOC) mice we have identified a deficit in recall of
Alessandro Graziano et al.
PloS one, 8(1), e54350-e54350 (2013-01-26)
Physical exercise promotes neural plasticity in the brain of healthy subjects and modulates pathophysiological neural plasticity after sensorimotor loss, but the mechanisms of this action are not fully understood. After spinal cord injury, cortical reorganization can be maximized by exercising
Chris Law et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 36(2), 561-576 (2016-01-14)
The role of synaptic activity during early formation of neural circuits is a topic of some debate; genetic ablation of neurotransmitter release by deletion of the Munc18-1 gene provides an excellent model to answer the question of whether such activity

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