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Specificity | TRK fused gene Rabbit Recombinant mAb detects endogenous level of total TRK fused gene. |
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Background | Trk-fused gene (TFG) is was initially identified as an oncogene causing thyroid cancer, in which the N-terminal half of TFG was fused with neurotrophic tyrosine kinase receptor 1 (NTRK1, also known as TrkA). Subsequently, TFG was also reported to be a fusion partner of the anaplastic lymphoma kinase (ALK) gene in anaplastic large cell lymphoma, though the function of TFG itself remained essentially unknown until quite recently. It was reported localized at endoplasmic reticulum (ER) exit sites (ERES) and to be crucial in transport from the ER to the Golgi apparatus via COPII vesicle. TFG is important for retention of COPII vesicles between the ER and ER-Golgi intermediate compartments (ERGIC), and in the absence of TFG, COPII-coated carriers become dispersed throughout the cytoplasm. On the other hand, TFG was recently identified as a causative gene for several neurodegenerative diseases, such as hereditary motor and sensory neuropathy with proximal dominant involvement (HMSN-P), the axonal type of Charcot-Marie-Tooth disease and hereditary spastic paraplegia (HSP). |
Application | WB,ELISA | ||
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Dilution |
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Reactivity | Human Mouse Rat | ||
MW (kDa) | 55kDa | ||
Source | Rabbit | ||
Concentration | 1mg/ml | ||
Storage buffer | 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. | ||
Storage (From the date of receipt) |
Store at –20°C. |
WB