anti-Signal-Regulatory Protein alpha (SIRPA) Antibodies

Human Signal-Regulatory Protein alpha (SIRPA) interaction partners

1. QPCTL is critical for pyroglutamate formation on CD47 at the SIRPalpha binding site shortly after biosynthesis.

2. Accumulation of SIRPalpha-inhibited macrophages in tumors favored tumor regression for 1-2 weeks, but donor macrophages quickly differentiated toward non-phagocytic, high-SIRPalpha TAMs.

3. SIRP alpha protein is under-expressed in low and high-grades of astrocytoma from patients' brain samples.

4. Anti-SIRPA antibody immunotherapy enhances neutrophil and macrophage antitumor activity.

5. SIRPalpha might play an important role in the progression of oral leukoplakia and oral cancer, and could be a pivotal therapeutic target in oral squamous cell carcinoma, regulating the phenotype of macrophages via targeting NF-kappaB signaling.

6. TTI-621 (SIRPalphaFc) is a fully human recombinant fusion protein that blocks the CD47-SIRPalpha axis by binding to human CD47 and enhancing phagocytosis of malignant cells..These data indicate that TTI-621 is active across a broad range of human tumors.

7. data suggest that TTI-621 may be efficacious in triggering the destruction of cancer cells by a diverse population of TAMs found in vivo and support possible combination approaches to augment the activity of CD47 blockade

8. CD47, TSP1, and to a lesser extent SIRPalpha facilitate exosome-mediated myeloid-derived suppressor cells chemotaxis and migration.

9. exploited by Hepatitis E virus to negative regulated IFN-beta of the host innate immune system to promote viral infection

10. Data suggest a reduction in the CD47 antigen/signal-regulatory protein alpha (SIRPalpha) pathway by programmed cell death protein 1 (PD-1) blockade, which regulates Myeloid-derived suppressor cells (MDSCs) and tumor associated macrophages (TAMs).

11. agents that block the CD47:SIRP-alpha engagement are attractive therapeutic targets as a monotherapy or in combination with additional immune-modulating agents for activating antitumor T cells in vivo

12. the data suggest that combinatorial actions of ADAM10 and gamma-secretase on SIRPalpha cleavage promote inflammatory signaling.

13. Loss of cell surface CD47 clustering formation and binding avidity to SIRPalpha facilitate apoptotic cell clearance by macrophages.

14. Velcro" engineering of high affinity CD47 ectodomain as signal regulatory protein alpha (SIRPalpha) antagonists that enhance antibody-dependent cellular phagocytosis

15. negatively regulates neutrophil accumulation during inflammation

16. Combinatorial expression of NKX2-5, SIRPA, VCAM1 and CD34 can be used to define discrete stages of cardiovascular cell lineage differentiation.

17. The independent non-obstructive azoospermia risk alleles are driven by variants in the protein-coding sequence of the two genes, SIRPA and SIRPG.

18. These results suggest that thrombospondin-1 binding to SIRP-alpha on nonphagocytic cells activates NADPH oxidase, limits vasodilation, and promotes renal ischemia reperfusion injury.

19. 'clustering' SIRPalpha into plasma membrane microdomains is essential for activated monocytes and macrophages to effectively interact with CD47 and initiate intracellular signaling

20. Polymorphisms in the human inhibitory signal-regulatory protein alpha do not affect binding to its ligand CD47.

Mouse (Murine) Signal-Regulatory Protein alpha (SIRPA) interaction partners

1. this study shows that miR-378a modulates macrophage phagocytosis and differentiation through targeting CD47-SIRPalpha axis in atherosclerosis

2. Data indicate that only signal regulatory protein alpha (SIRPalpha+) CD8(+) T cells actively proliferate and show cytolytic activity.

3. Microglia are effector cells of CD47-SIRPalpha antiphagocytic axis disruption against glioblastoma.

4. Tyrosine phosphorylation of SIRPalpha is necessary for SIRPalpha cleavage and presynaptic maturation.

5. Accumulation of SIRPalpha-inhibited macrophages in tumors favored tumor regression for 1-2 weeks, but donor macrophages quickly differentiated toward non-phagocytic, high-SIRPalpha TAMs.

6. Anti-SIRPA antibody immunotherapy enhances neutrophil and macrophage antitumor activity.

7. SIRPalpha-expressing dendritic cells regulate homeostasis of fibroblastic reticular cells via TNF receptor ligands in the adult mouse spleen.

8. CCR7 deficiency results in apoptosis of Sirpa- dendritic cells, which is counterbalanced by expansion of immature Sirpa+ dendritic cells that efficiently induce Treg generation.

9. Mechanistic studies suggest a PKC-Syk-mediated signaling pathway, to which IL-10 conversely inhibits, is required for activating macrophage self-targeting, followed by phagocytosis independent of calreticulin Moreover, we identified spleen red pulp to be one specific tissue that provides stimuli constantly activating macrophage phagocytosis albeit lacking in Cd47(-/-) or Sirpalpha(-/-) mice.

10. these findings have demonstrated how tumor cells inhibit innate sensing in dendritic cells and suggested that the CD47-SIRPalpha axis is critical for dendritic cell-driven antitumor immunity

11. Data provide evidence that SIRPalpha-mediated phagocytosis is not a major determinant in prion disease pathogenesis.

12. Treg cells protect dopaminergic neurons against MPP+ neurotoxicity by a cell-to-cell contact mechanism underlying CD47-SIRPA interaction and Rac1/Akt activation.

13. In conclusion, our data suggest that SIRPalpha signaling through SHP-2-PI3K-Akt2 strongly influences osteoblast differentiation from bone marrow stromal cells.

14. These results indicate an important role for CD47-SIRPalpha interactions in innate control of malaria and suggest novel targets for intervention.

15. TLR5 mediates CD172a(+) intestinal lamina propria dendritic cell induction of Th17 cells.

16. a novel and opposite contribution of SIRPalpha signaling within non-hematopoietic and hematopoietic cells

17. These findings demonstrate, for the first time, that SIRPalpha signaling can directly control phagocyte migration.

18. SIRPalpha intrinsic to CD11c(+) dendritic cells is essential for homeostasis of conventional dendritic cells in the secondary lymphoid organs and skin.

19. Loss of cell surface CD47 clustering formation and binding avidity to SIRPalpha facilitate apoptotic cell clearance by macrophages.

20. data identified SIRPalpha signaling in non-hematopoietic cells to play an important role in regulating the numbers and positioning MZB cell in the spleen