Phospho-TrkA (Y785)/TrkB (Y816) Antibody [G6J11]

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000

Application
WB

Reactivity
Human

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
140 kDa

Datasheet & SDS

Biological Description

Specificity
Phospho-TrkA (Y785)/TrkB (Y816) Antibody [G6J11] detects endogenous levels of total TrkA and TrkB protein only when it is phosphorylated at Y785 and Y816, respectively.

Clone
G6J11

Synonym(s)
High affinity nerve growth factor receptor; Neurotrophic tyrosine kinase receptor type 1; Tyrosine kinase receptor A (Trk-A); gp140trk 1; p140-TrkA; NTRK1; MTC; TRK; TRKA; BDNF/NT-3 growth factors receptor

Background
Phospho-TrkA (Y785)/TrkB (Y816) refers to a conserved phosphotyrosine site in the C-terminal intracellular tail of Trk receptor tyrosine kinases (TrkA, TrkB, TrkC family), activated by neurotrophins, NGF for TrkA and BDNF/NT4 for TrkB, regulating neuronal survival, differentiation, synaptic plasticity, and axon growth via dimerization and kinase autophosphorylation. TrkA features an extracellular ligand-binding domain, a single transmembrane helix, a juxtamembrane region, a protein kinase domain (with activation loop tyrosines like Y674/675), and a C-terminal tail containing Y785 (equivalent to Y816 in TrkB), which, upon phosphorylation, docks phospholipase Cγ1 (PLCγ) via its SH2 domain, distinct from the Y490 Shc-binding site. Phosphorylation at Y785/pY816 primarily activates PLCγ, triggering IP3-mediated Ca2+ release, PKC activation, and subsequent Ras-MAPK/ERK signaling for neurite outgrowth, cell cycle regulation, and gene transcription, while also influencing neuronal excitability and synaptic strengthening independent of MAPK pathways activated by other sites. Aberrant phosphorylation drives oncogenic signaling in neuroblastomas and other cancers via ligand-independent dimerization, while in the nervous system, it supports adult synaptic plasticity but hyperactivation contributes to chronic pain and neurodegeneration. Mutations disrupting Y785 abolish PLCγ responses without affecting Shc/MAPK.

Background

Phospho-TrkA (Y785)/TrkB (Y816) refers to a conserved phosphotyrosine site in the C-terminal intracellular tail of Trk receptor tyrosine kinases (TrkA, TrkB, TrkC family), activated by neurotrophins, NGF for TrkA and BDNF/NT4 for TrkB, regulating neuronal survival, differentiation, synaptic plasticity, and axon growth via dimerization and kinase autophosphorylation. TrkA features an extracellular ligand-binding domain, a single transmembrane helix, a juxtamembrane region, a protein kinase domain (with activation loop tyrosines like Y674/675), and a C-terminal tail containing Y785 (equivalent to Y816 in TrkB), which, upon phosphorylation, docks phospholipase Cγ1 (PLCγ) via its SH2 domain, distinct from the Y490 Shc-binding site. Phosphorylation at Y785/pY816 primarily activates PLCγ, triggering IP3-mediated Ca2+ release, PKC activation, and subsequent Ras-MAPK/ERK signaling for neurite outgrowth, cell cycle regulation, and gene transcription, while also influencing neuronal excitability and synaptic strengthening independent of MAPK pathways activated by other sites. Aberrant phosphorylation drives oncogenic signaling in neuroblastomas and other cancers via ligand-independent dimerization, while in the nervous system, it supports adult synaptic plasticity but hyperactivation contributes to chronic pain and neurodegeneration. Mutations disrupting Y785 abolish PLCγ responses without affecting Shc/MAPK.

References
https://pubmed.ncbi.nlm.nih.gov/14662744/ https://pubmed.ncbi.nlm.nih.gov/20445044/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

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%