Polyclonal Anti-Trk-A

Rabbit IgG polyclonal antibody for High affinity nerve growth factor receptor ( NTRK1) detection. Tested with WB, IHC-P in Human;Mouse;Rat. \n

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SPECIFICATIONS

Price

200.00 USD

Catalog Number

PA1321

Size

100ug/vial

Applications

IHC, WB

Reactivities

Hum, Mouse, Rat

Form

Lyophilized

Format

Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg Thimerosal, 0.05mg NaN3.

Gene Id

NTRK1

References

1. Lambiase A, Merlo D, Mollinari C, Bonini P, Rinaldi AM, D' Amato M, Micera A, Coassin M, Rama P, Bonini S, Garaci E (November 2005). \"Molecular basis for keratoconus: lack of TrkA expression and its transcriptional repression by Sp3\". Proc. Natl. Acad. Sci. U.S.A.102 (46): 16795

Swiss Prot

P04629

Storage Temp

\"At -20 degree C for one year. After reconstitution, at 4 degree C for one month. It can also be aliquotted and stored frozen at -20 degree C for a longer time.\nAvoid repeated freezing and thawing. \n\"\n

Additional Info

A synthetic peptide corresponding to a sequence in the middle region of human NTRK1, identical to the related rat and mouse sequences.

Scientific Background

Trk A (Neurotrophic tyrosine kinase receptor A) is the high affinity catalytic receptor for the neurotrophin, Nerve Growth Factor (NGF). Higher affinity binding of NGFR can achieved by association with higher molecular mass, low-affinity neurotrophin receptors, namely the tropomyosin receptor kinases, TRKA (NTRK1), TRKB (NTRK2), and TRKC (NTRK3). TRKA, TRKB, and TRKC are specific for or 'preferred by' NGF, NTF4(Neurotrophin-4) and BDNF, and NTF3(Neurotrophin-3), respectively. NTF3 also binds to TRKA and TRKB, but with significantly lower affinity. The absence of TrkA(NGFR) expression was associated with a strong increase in the Sp3 repressor short isoform(s) and a lack of the Sp3 activator long isoform. Sp3 is a bifunctional transcription factor that has been reported to stimulate or repress the transcription of numerous genes. Indo et al. (1996) concluded that defects in TRKA cause CIPA (Congenital insensitivity to pain with anhidrosis ) and that the NGF-TRKA system has a crucial role in the development and function of the nociceptive reception as well as establishment of thermoregulation via sweating in humans. These results also implicate genes encoding other TRK and neurotrophin family members as candidates for developmental defect(s) of the nervous system.