|83163T||1 Kit (9 x 20 microliters)||
|ASC/TMS1 (D2W8U) Rabbit mAb 67824||20 µl||
|HS1 (D5A9) XP® Rabbit mAb 3892||20 µl||
||M R||80||Rabbit IgG|
|Ki-67 (D3B5) Rabbit mAb 9129||20 µl||
||H M R||359||Rabbit IgG|
|Axl (C89E7) Rabbit mAb 8661||20 µl||
||H Mk||138||Rabbit IgG|
|Hydroxy-HIF-1α (Pro564) (D43B5) XP® Rabbit mAb 3434||20 µl||
||H Mk||120||Rabbit IgG|
|Stat2 (D9J7L) Rabbit mAb 72604||20 µl||
||H M||97, 113||Rabbit IgG|
|Phospho-Stat2 (Tyr690) (D3P2P) Rabbit mAb 88410||20 µl||
||H R||97, 113||Rabbit IgG|
|Lamin A/C (4C11) Mouse mAb 4777||20 µl||
||H M R Mk||74 (Lamin A), 63 (Lamin C)||Mouse IgG2a|
|IQGAP1 (D8K4X) XP® Rabbit mAb 20648||20 µl||
||H M R Mk||195||Rabbit IgG|
|Anti-rabbit IgG, HRP-linked Antibody 7074||100 µl||
Monoclonal antibodies are produced by immunizing animals with synthetic peptides corresponding to residues surrounding Leu310 of mouse HS1, Pro564 of human HIF-1α, Leu706 of human Stat2, Tyr690 of human Stat2, the amino terminus of human Ki-67 and IQGAP1, and recombinant fragment of human Axl, human lamin A, and mouse ASC/TMS1.
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).
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