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Nerve growth factor stimulates MAPK via the low affinity receptor p75 LNTR
Author(s) -
Susen Kathrin,
Heumann Rolf,
Blöchl Andrea
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01628-2
Subject(s) - tropomyosin receptor kinase a , nerve growth factor , trk receptor , mapk/erk pathway , low affinity nerve growth factor receptor , protein kinase a , microbiology and biotechnology , chemistry , kinase , ceramide , mapk cascade , mitogen activated protein kinase , receptor , biology , biochemistry , apoptosis
Apart from its high affinity receptor TrkA, nerve growth factor (NGF) can also stimulate the low affinity receptor p75 LNTR and induce a Trk‐independent signaling cascade. We examined the possible involvement of mitogen‐activated protein kinase (MAPK) in this signaling pathway in neuronal cultures of the cerebellum of P2‐aged rats and PCNA cells; both cell types express p75 LNTR but not TrkA. We found a fast and transient phosphorylation of p42‐ and p44‐MAPK after stimulation with NGF or C 2 ‐ceramide which proved to be sensitive to inhibition of MAPK kinase and protein kinase A (PKA). As stimulation with NGF also activated p21Ras it can be concluded that at least part of the observed MAPK activation was effected via p21Ras and via PKA.