Microglia Cross Module Antibody Sampler Kit

Distinct microglial activation states have been identified using RNA-seq data from a vast array of neurological disease and aging models. These activation states have been categorized into modules corresponding to proliferation, neurodegeneration, interferon-relation, LPS-relation, and many others (1). Previous work identifying markers of specific brain cell types using RNA-seq has shown HS1 and ASC/TMS1 to be useful and specific tools to study microglia (2). HS1 is a protein kinase substrate that is expressed only in tissues and cells of hematopoietic origin (3) and ASC/TMS1 has been found to be a critical component of inflammatory signaling where it associates with and activates caspase-1 in response to pro-inflammatory signals (4).Ki-67 is a nuclear nonhistone protein (5) universally expressed among proliferating cells and absent in quiescent cells (6). Axl is a receptor tyrosine kinase that binds Gas6, stimulating regulatory effects on microglial phagocytic response to inflammatory stimuli (7). Hypoxia inducible factor-1 (HIF-1α) is a transcription factor responsible for adaptation to low oxygen environments whose downstream effects have been shown in a number of neurodegenerative diseases. Under normoxic conditions, HIF-1α is proline hydroxylated leading to ubiquitin mediated degradation (8). Stat2 is critical to the transcriptional responses induced by type I interferons, IFN-alpha/beta (9,10). In response to IFN-alpha/beta, Stat2 is activated by phosphorylation at site Tyr690 through associations with receptor-bound Jak kinases (11). Lamins are nuclear membrane structural components important for maintaining normal cell functions. Lamin A/C is cleaved by caspase-6 and serves as a marker for caspase-6 activation. The cleavage of lamins results in nuclear dysregulation and cell death (12,13). IQGAP1 is ubiquitously expressed and has been found to interact with APC (14) and the CLIP170 complex in response to small GTPases, promoting cell polarization and migration (15). 1.Friedman, B.A. et al. (2018) Cell Rep 22, 832-47. 2.Zhang, Y. et al. (2014) J Neurosci 34, 11929-47. 3.Kitamura, D. et al. (1995) Biochem Biophys Res Commun 208, 1137-46. 4.Srinivasula, S.M. et al. (2002) J Biol Chem 277, 21119-22. 5.Gerdes, J. et al. (1983) Int J Cancer 31, 13-20. 6.Weigel, M.T. and Dowsett, M. (2010) Endocr Relat Cancer 17, R245-62. 7.Grommes, C. et al. (2008) J Neuroimmune Pharmacol 3, 130-40. 8.Zhang, Z. et al. (2011) Curr Med Chem 18, 4335-43. 9.Fu, X.Y. et al. (1992) Proc Natl Acad Sci U S A 89, 7840-3. 10.Ihle, J.N. (2001) Curr Opin Cell Biol 13, 211-7. 11.Improta, T. et al. (1994) Proc Natl Acad Sci U S A 91, 4776-80. 12.Oberhammer, F.A. et al. (1994) J Cell Biol 126, 827-37. 13.Rao, L. et al. (1996) J Cell Biol 135, 1441-55. 14.Watanabe, T. et al. (2004) Dev Cell 7, 871-83. 15.Fukata, M. et al. (2002) Cell 109, 873-85.