| protection from experimental cerebral malaria pathology in Irgm3-/- mice occurs due to impaired generation of CD8+ effector function. This defect is nonintrinsic to CD8+ T cells. | IRGM3 contributes to immunopathology and is required for differentiation of antigen-specific effector CD8+ T cells in experimental cerebral malaria.
Guo J, McQuillan JA, Yau B, Tullo GS, Long CA, Bertolino P, Roediger B, Weninger W, Taylor GA, Hunt NH, Ball HJ, Mitchell AJ., Free PMC Article | 07/25/2015 |
| the paralogous IRGM proteins Irgm1 and Irgm3 fail to robustly associate with "non-self" PVs containing either the bacterial pathogen Chlamydia trachomatis or the protozoan pathogen Toxoplasma gondii | IRG and GBP host resistance factors target aberrant, "non-self" vacuoles characterized by the missing of "self" IRGM proteins.
Haldar AK, Saka HA, Piro AS, Dunn JD, Henry SC, Taylor GA, Frickel EM, Valdivia RH, Coers J., Free PMC Article | 01/18/2014 |
| IRGM proteins indirectly modulate the localization of GBP2 through a distinct mechanism from that through which they regulate IRG protein localization | Immunity-related GTPase M (IRGM) proteins influence the localization of guanylate-binding protein 2 (GBP2) by modulating macroautophagy.
Traver MK, Henry SC, Cantillana V, Oliver T, Hunn JP, Howard JC, Beer S, Pfeffer K, Coers J, Taylor GA., Free PMC Article | 10/29/2011 |
| Data show that hyperproliferation, self-renewal, and autophagy defects in Irgm1(-/-) HSCs were normalized in double-knockout Irgm1(-/-)Ifngr1(-/-) and Irgm1(-/-)Stat1(-/-), and the defects were abolished in Irgm1(-/-)Irgm3(-/-) double-knockout. | Irgm1 protects hematopoietic stem cells by negative regulation of IFN signaling.
King KY, Baldridge MT, Weksberg DC, Chambers SM, Lukov GL, Wu S, Boles NC, Jung SY, Qin J, Liu D, Songyang Z, Eissa NT, Taylor GA, Goodell MA., Free PMC Article | 10/22/2011 |
| IFN-gamma-inducible signaling has pleiotropic effects on immune defense and revealing that p47 GTPases function differentially depending on invading pathogen species. | IFN-inducible p47 GTPases display differential responses to Schistosoma japonicum acute infection.
Chen X, Du X, Zhang M, Zhang D, Ji M, Wu G., Free PMC Article | 03/15/2010 |
| Irgm3 is stimulated by interferon-gamma, and functions to counter the effects of Irgm1. | Balance of Irgm protein activities determines IFN-gamma-induced host defense.
Henry SC, Daniell XG, Burroughs AR, Indaram M, Howell DN, Coers J, Starnbach MN, Hunn JP, Howard JC, Feng CG, Sher A, Taylor GA., Free PMC Article | 01/21/2010 |
| Immunity-related GTPase (IRG) family member Irgm3 is required for the ability of in vivo primed macrophages to restrain the growth of Toxoplasma gondii and to destroy the parasite's intracellular niche. | Virulent Toxoplasma gondii evade immunity-related GTPase-mediated parasite vacuole disruption within primed macrophages.
Zhao Y, Ferguson DJ, Wilson DC, Howard JC, Sibley LD, Yap GS., Free PMC Article | 01/21/2010 |
| Vacuolar disruption in T. gondii infected murine astrocytes was found to be dependent upon IFN-gamma-inducible GTP-binding protein | The gamma interferon (IFN-gamma)-inducible GTP-binding protein IGTP is necessary for toxoplasma vacuolar disruption and induces parasite egression in IFN-gamma-stimulated astrocytes.
Melzer T, Duffy A, Weiss LM, Halonen SK., Free PMC Article | 01/21/2010 |
| Focal adhesion kinase is phosphorylated in response to interferon-gamma-inducible GTPase expression. | Focal adhesion kinase mediates the interferon-gamma-inducible GTPase-induced phosphatidylinositol 3-kinase/Akt survival pathway and further initiates a positive feedback loop of NF-kappaB activation.
Liu Z, Zhang HM, Yuan J, Lim T, Sall A, Taylor GA, Yang D., Free PMC Article | 01/21/2010 |
| Differential induction by various gram-negative lipopolysaccharides was myeloid differentiation factor 88 (MyD88)-independent | Differential inductions of TNF-alpha and IGTP, IIGP by structurally diverse classic and non-classic lipopolysaccharides.
Lapaque N, Takeuchi O, Corrales F, Akira S, Moriyon I, Howard JC, Gorvel JP. | 01/21/2010 |
| IGTP has a role in cell survival which relies on activation of PI3-K/Akt, inactivation of GSK-3 and suppression of caspase-9 and caspase-3 | Overexpression of interferon-gamma-inducible GTPase inhibits coxsackievirus B3-induced apoptosis through the activation of the phosphatidylinositol 3-kinase/Akt pathway and inhibition of viral replication.
Zhang HM, Yuan J, Cheung P, Luo H, Yanagawa B, Chau D, Stephan-Tozy N, Wong BW, Zhang J, Wilson JE, McManus BM, Yang D. | 01/21/2010 |
| Function of IGTp in host resistance to Toxoplasma gondii is stat1 dependent and requires expression in both hematopoietic and nonhematopoietic cellular compartments | The function of gamma interferon-inducible GTP-binding protein IGTP in host resistance to Toxoplasma gondii is Stat1 dependent and requires expression in both hematopoietic and nonhematopoietic cellular compartments.
Collazo CM, Yap GS, Hieny S, Caspar P, Feng CG, Taylor GA, Sher A., Free PMC Article | 01/21/2010 |
| Data use fine structure mapping in congenic fibroblasts carrying DNA from the susceptible parent to localize the effect of Ctrq-3 to a 1.2-megabase interval of genomic DNA that contains Irgb10 and Igtp. | The p47 GTPases Igtp and Irgb10 map to the Chlamydia trachomatis susceptibility locus Ctrq-3 and mediate cellular resistance in mice.
Bernstein-Hanley I, Coers J, Balsara ZR, Taylor GA, Starnbach MN, Dietrich WF., Free PMC Article | 01/21/2010 |