Expression of the v-crk oncogene product in PC12 cells results in rapid differentiation by both nerve growth factor- and epidermal growth factor-dependent pathways - PubMed (original) (raw)
Expression of the v-crk oncogene product in PC12 cells results in rapid differentiation by both nerve growth factor- and epidermal growth factor-dependent pathways
B L Hempstead et al. Mol Cell Biol. 1994 Mar.
Abstract
The transforming gene of the avian sarcoma virus CT10 encodes a fusion protein (p47gag-crk or v-Crk) containing viral Gag sequences fused to cellular sequences consisting primarily of Src homology regions 2 and 3 (SH2 and SH3 sequences). Here we report a novel function of v-Crk in the mammalian pheochromocytoma cell line, PC12, whereby stable expression of v-Crk induces accelerated differentiation, as assessed by induction of neurites following nerve growth factor (NGF) or basic fibroblast growth factor (bFGF) treatment compared with the effect in native PC12 cells. Surprisingly, however, these cells also develop extensive neurite processes after epidermal growth factor (EGF) stimulation, an event which is not observed in native PC12 cells. Following EGF or NGF stimulation of the v-CrkPC12 cells, the v-Crk protein itself became tyrosine phosphorylated within 1 min. Moreover, in A431 cells or TrkA-PC12 cells, which overexpress EGF receptors and TrkA, respectively, a GST-CrkSH2 fusion protein was indeed capable of binding these receptors in a phosphotyrosine-dependent manner, suggesting that v-Crk can directly couple to receptor tyrosine kinase pathways in PC12 cells. In transformed fibroblasts, v-Crk binds to specific tyrosine-phosphorylated proteins of p130 and paxillin. Both of these proteins are also complexed to v-Crk in PC12 cells, as evidenced by their coprecipitation with v-Crk in detergent lysates, suggesting that common effector pathways may occur in both cell types. However, whereas PC12 cellular differentiation can occur solely by overexpression of the v-Src or oncogenic Ras proteins, that induced by v-Crk requires a growth factor stimulatory signal, possibility in a two-step process.
Similar articles
- Identification and characterization of a high-affinity interaction between v-Crk and tyrosine-phosphorylated paxillin in CT10-transformed fibroblasts.
Birge RB, Fajardo JE, Reichman C, Shoelson SE, Songyang Z, Cantley LC, Hanafusa H. Birge RB, et al. Mol Cell Biol. 1993 Aug;13(8):4648-56. doi: 10.1128/mcb.13.8.4648-4656.1993. Mol Cell Biol. 1993. PMID: 7687742 Free PMC article. - v-Crk modulation of growth factor-induced PC12 cell differentiation involves the Src homology 2 domain of v-Crk and sustained activation of the Ras/mitogen-activated protein kinase pathway.
Teng KK, Lander H, Fajardo JE, Hanafusa H, Hempstead BL, Birge RB. Teng KK, et al. J Biol Chem. 1995 Sep 1;270(35):20677-85. doi: 10.1074/jbc.270.35.20677. J Biol Chem. 1995. PMID: 7657647 - Nerve growth factor stimulates the tyrosine phosphorylation of endogenous Crk-II and augments its association with p130Cas in PC-12 cells.
Ribon V, Saltiel AR. Ribon V, et al. J Biol Chem. 1996 Mar 29;271(13):7375-80. doi: 10.1074/jbc.271.13.7375. J Biol Chem. 1996. PMID: 8631760 - Physiological signals and oncogenesis mediated through Crk family adapter proteins.
Feller SM, Posern G, Voss J, Kardinal C, Sakkab D, Zheng J, Knudsen BS. Feller SM, et al. J Cell Physiol. 1998 Dec;177(4):535-52. doi: 10.1002/(SICI)1097-4652(199812)177:4<535::AID-JCP5>3.0.CO;2-E. J Cell Physiol. 1998. PMID: 10092207 Review. - Emerging components of the Crk oncogene product: the first identified adaptor protein.
Matsuda M, Kurata T. Matsuda M, et al. Cell Signal. 1996 Aug;8(5):335-40. doi: 10.1016/0898-6568(96)00067-8. Cell Signal. 1996. PMID: 8911681 Review.
Cited by
- CRKL but not CRKII contributes to hemin-induced erythroid differentiation of CML.
Guo C, Lv X, Zhang Q, Yi L, Ren Y, Li Z, Yan J, Zheng S, Sun MZ, Liu S. Guo C, et al. J Cell Mol Med. 2024 May;28(9):e18308. doi: 10.1111/jcmm.18308. J Cell Mol Med. 2024. PMID: 38683131 Free PMC article. - The Effect of Interaction NGF/p75NTR in Sperm Cells: A Rabbit Model.
Castellini C, Mattioli S, Cotozzolo E, Pistilli A, Rende M, Bartolini D, Di Sante G, Menchetti L, Dal Bosco A, Stabile AM. Castellini C, et al. Cells. 2022 Mar 18;11(6):1035. doi: 10.3390/cells11061035. Cells. 2022. PMID: 35326486 Free PMC article. - Proteomics analysis of fetal growth restriction and taurine‑treated fetal growth restriction rat brain tissue by 2D DIGE and MALDI‑TOF/TOF MS analysis.
Liu H, Wang Y, Liu J, Fu W. Liu H, et al. Int J Mol Med. 2019 Jul;44(1):207-217. doi: 10.3892/ijmm.2019.4182. Epub 2019 May 7. Int J Mol Med. 2019. PMID: 31115483 Free PMC article. - Crk II silencing down-regulates IGF-IR and inhibits migration and invasion of prostate cancer cells.
Dhupkar P, Zhao H, Mujoo K, An Z, Zhang N. Dhupkar P, et al. Biochem Biophys Rep. 2016 Oct 28;8:382-388. doi: 10.1016/j.bbrep.2016.10.009. eCollection 2016 Dec. Biochem Biophys Rep. 2016. PMID: 28955980 Free PMC article. - The signaling adapter, FRS2, facilitates neuronal branching in primary cortical neurons via both Grb2- and Shp2-dependent mechanisms.
Zhou L, Talebian A, Meakin SO. Zhou L, et al. J Mol Neurosci. 2015 Mar;55(3):663-77. doi: 10.1007/s12031-014-0406-4. Epub 2014 Aug 27. J Mol Neurosci. 2015. PMID: 25159185
References
- Proc Natl Acad Sci U S A. 1976 Jul;73(7):2424-8 - PubMed
- Nature. 1986 Feb 20-26;319(6055):680-2 - PubMed
- Cell. 1981 Jun;24(3):867-74 - PubMed
- J Neurosci. 1985 Feb;5(2):307-16 - PubMed
- Genes Dev. 1990 May;4(5):683-94 - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Research Materials
Miscellaneous