Research Topics
Genomes and GenesSpecies | Amir A Sadighi AkhaSummaryAffiliation: University of Michigan Country: USA Publications
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Detail Information
Publications
Heightened induction of proapoptotic signals in response to endoplasmic reticulum stress in primary fibroblasts from a mouse model of longevityAmir A Sadighi Akha
Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA
J Biol Chem 286:30344-51. 2011..These results, together with recent findings in Caenorhabditis elegans daf-2 mutants, point to a potential interplay between insulin/IGF-1 signals and unfolded protein response signaling...
Enhancement of CD8 T-cell function through modifying surface glycoproteins in young and old miceAmir A Sadighi Akha
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109 2200, USA
Immunology 119:187-94. 2006....
CD43-independent augmentation of mouse T-cell function by glycoprotein cleaving enzymesScott B Berger
Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, MI 48109 2200, USA
Immunology 119:178-86. 2006..The preferential ability of PNGase F and ST-Siase(2,3) to improve the function of T cells from aged mice may involve cleavage of glycoproteins containing alpha2,3-linked sialic acid residues on N-linked or O-linked glycans or both...
A glycoprotein endopeptidase enhances calcium influx and cytokine production by CD4+ T cells of old and young miceScott B Berger
Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, MI, USA
Int Immunol 17:983-91. 2005..These data support a model in which O-glycosylated surface proteins inhibit CD4+ lymphocyte activation in both young and old mice, and in which such glycoproteins contribute to the age-related decline in cytokine production...
Age-related defects in moesin/ezrin cytoskeletal signals in mouse CD4 T cellsGonzalo G Garcia
Department of Pathology, University of Michigan School of Medicine, Ann Arbor, MI 48109, USA
J Immunol 179:6403-9. 2007..In addition, CD4 T cells from aged mice show defects in the Rho GTPase activities known to control ERM function...
Life-span extension in mice by preweaning food restriction and by methionine restriction in middle ageLiou Sun
Department of Pathology and Geriatrics Center, University of Michigan, Ann Arbor, 48109 2200, USA
J Gerontol A Biol Sci Med Sci 64:711-22. 2009..These results introduce new protocols that can increase maximal life span and suggest that the spectrum of metabolic changes induced by low-calorie and low-methionine diets may differ in instructive ways...
T cells in aging mice: genetic, developmental, and biochemical analysesRichard A Miller
Department of Pathology, University of Michigan School of Medicine, Ann Arbor, 48109, USA
Immunol Rev 205:94-103. 2005....
Fibroblasts from naked mole-rats are resistant to multiple forms of cell injury, but sensitive to peroxide, ultraviolet light, and endoplasmic reticulum stressAdam B Salmon
Cellular and Molecular Biology Graduate Program, University of Michigan, Ann Arbor, MI, USA
J Gerontol A Biol Sci Med Sci 63:232-41. 2008..The sensitivity of both Snell dwarf and NMR cells to ER stress suggests that alterations in the unfolded protein response might modulate cell survival and aging rate...
Age-associated changes in glycosylation of CD43 and CD45 on mouse CD4 T cellsGonzalo G Garcia
Department of Pathology, University of Michigan School of Medicine, Ann Arbor, MI, USA
Eur J Immunol 35:622-31. 2005..These data support the idea that changes in T cell surface glycosylation could play an important role in immune senescence...
Signal transduction in the aging immune systemAmir A Sadighi Akha
Department of Veterans Affairs Medical Center, Ann Arbor, Michigan 48109-0940, USA
Curr Opin Immunol 17:486-91. 2005..Evidence for intrinsic signal defects in aged B cells is more limited, but might involve pathways that activate the transcription factor E47, which has been implicated in somatic hypermutation and class-switch recombination...
Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteinsD Thomas Rutkowski
Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor, Michigan, USA
PLoS Biol 4:e374. 2006..It underscores the contribution of posttranscriptional and posttranslational mechanisms in influencing this outcome...
