Data on isoaspartylation of neuronal ELAVL proteins

Data in Brief

Ite A. Laird-Offringa¹  Meleeneh Kazarian DerHartunian¹  Mario A. Pulido¹  Prerna Sehgal¹ 

[1] Departments of Surgery and of Biochemistry and Molecular Medicine, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA;

关键词: Auto-antigens;    Autoimmunity;    ELAVL;    Isoaspartylation;    Neuronal proteins;    Small cell lung cancer;    SCLC;   

DOI  :  10.1016/j.dib.2016.11.034

来源: DOAJ

【 摘 要 】

This article contains experimental data examining the propensity of neuronal ELAVL proteins to become isoaspartylated. The data are related to the article “Isoaspartylation appears to trigger small cell lung cancer-associated autoimmunity against neuronal protein ELAVL4” (M.A. Pulido, M.K. DerHartunian, Z. Qin, E.M. Chung, D.S. Kang, A.W. Woodham, J.A. Tsou, R. Klooster, O. Akbari, L. Wang, W.M. Kast, S.V. Liu, J.J.G.M. Verschuuren, D.W. Aswad, I.A. Laird-Offringa, 2016) [1], in which it was reported that the N-terminal region of recombinant human ELAVL4 protein, incubated under physiological conditions, acquires a type of highly immunogenic protein damage. Here, we present Western blot analysis data generated by using an affinity-purified polyclonal rabbit antibody (raised against an N-terminal ELAVL4 isoaspartyl-converted peptide) to probe recombinant protein fragments of the other three members of the ELAVL family: the highly homologous neuronal ELAVL2 (HuB) and ELAVL3 (HuC), and the much less homologous ubiquitously expressed ELAVL1 (HuR).

【 授权许可】

Unknown