Person:
Strominger, Jack

Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Strominger

First Name

Jack

Name

Strominger, Jack

Filters

2002 - 200912010 - 20172

Settings

Author's Publications: search.filters.isAuthorOfPublication.583ec1b6-8b75-473d-bda2-06bad2c146a3

Search Results

Now showing 1 - 3 of 3
  • Thumbnail Image
    Publication
    Disulfide bond-mediated dimerization of HLA-G on the cell surface
    (Proceedings of the National Academy of Sciences, 2002) Boyson, J. E.; Erskine, R.; Whitman, Mary; Chiu, Michael; Lau, J. M.; Koopman, L. A.; Valter, M. M.; Angelisova, P.; Horejsi, V.; Strominger, Jack
    HLA-G is a nonclassical class I MHC molecule with an unknown function and with unusual characteristics that distinguish it from other class I MHC molecules. Here, we demonstrate that HLA-G forms disulfide-linked dimers that are present on the cell surface. Immunoprecipitation of HLA-G from surface biotinylated transfec- tants using the anti-[]2-microglobulin mAb BBM.1 revealed the presence of an []78-kDa form of HLA-G heavy chain that was reduced by using DTT to a 39-kDa form. Mutation of Cys-42 to a serine completely abrogated dimerization of HLA-G, suggesting that the disulfide linkage formed exclusively through this residue. A possible interaction between the HLA-G monomer or dimer and the KIR2DL4 receptor was also investigated, but no interaction between these molecules could be detected through several approaches. The cell-surface expression of dimerized HLA-G molecules may have implications for HLA-G[]receptor interactions and for the search for specific receptors that bind HLA-G.
  • Thumbnail Image
    Publication
    Transcriptome analysis reveals similarities between human blood CD3− CD56bright cells and mouse CD127+ innate lymphoid cells
    (Nature Publishing Group UK, 2017) Allan, David S. J.; Cerdeira, Ana Sofia; Ranjan, Anuisa; Kirkham, Christina L.; Aguilar, Oscar A.; Tanaka, Miho; Childs, Richard W.; Dunbar, Cynthia E.; Strominger, Jack; Kopcow, Hernan D.; Carlyle, James R.
    For many years, human peripheral blood natural killer (NK) cells have been divided into functionally distinct CD3− CD56bright CD16− and CD3− CD56dim CD16+ subsets. Recently, several groups of innate lymphoid cells (ILC), distinct from NK cells in development and function, have been defined in mouse. A signature of genes present in mouse ILC except NK cells, defined by Immunological Genome Project studies, is significantly over-represented in human CD56bright cells, by gene set enrichment analysis. Conversely, the signature genes of mouse NK cells are enriched in human CD56dim cells. Correlations are based upon large differences in expression of a few key genes. CD56bright cells show preferential expression of ILC-associated IL7R (CD127), TNFSF10 (TRAIL), KIT (CD117), IL2RA (CD25), CD27, CXCR3, DPP4 (CD26), GPR183, and MHC class II transcripts and proteins. This could indicate an ontological relationship between human CD56bright cells and mouse CD127+ ILC, or conserved networks of transcriptional regulation. In line with the latter hypothesis, among transcription factors known to impact ILC or NK cell development, GATA3, TCF7 (TCF-1), AHR, SOX4, RUNX2, and ZEB1 transcript levels are higher in CD56bright cells, while IKZF3 (AIOLOS), TBX21 (T-bet), NFIL3 (E4BP4), ZEB2, PRDM1 (BLIMP1), and RORA mRNA levels are higher in CD56dim cells.
  • Thumbnail Image
    Publication
    Monitoring peripheral nerve degeneration in ALS by label-free stimulated Raman scattering imaging
    (Nature Publishing Group, 2016) Tian, Feng; Yang, Wenlong; Mordes, Daniel; Wang, Jin-Yuan; Salameh, Johnny S.; Mok, Woon Jong Joanie; Chew, Jeannie; Sharma, Aarti; Leno-Duran, Ester; Suzuki-Uematsu, Satomi; Suzuki, Naoki; Han, Steve S.; Lu, Fa-Ke; Ji, Minbiao; Zhang, Rosanna; Liu, Yue; Strominger, Jack; Shneider, Neil A.; Petrucelli, Leonard; Xie, X. Sunney; Eggan, Kevin
    The study of amyotrophic lateral sclerosis (ALS) and potential interventions would be facilitated if motor axon degeneration could be more readily visualized. Here we demonstrate that stimulated Raman scattering (SRS) microscopy could be used to sensitively monitor peripheral nerve degeneration in ALS mouse models and ALS autopsy materials. Three-dimensional imaging of pre-symptomatic SOD1 mouse models and data processing by a correlation-based algorithm revealed that significant degeneration of peripheral nerves could be detected coincidentally with the earliest detectable signs of muscle denervation and preceded physiologically measurable motor function decline. We also found that peripheral degeneration was an early event in FUS as well as C9ORF72 repeat expansion models of ALS, and that serial imaging allowed long-term observation of disease progression and drug effects in living animals. Our study demonstrates that SRS imaging is a sensitive and quantitative means of measuring disease progression, greatly facilitating future studies of disease mechanisms and candidate therapeutics.