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关键词:'I17001'
显示 1-9 共 9 条结果 关于 "I17001" 范围 论文
Hiroshi Nomoto et al.
Diabetologia, 63(1), 149-161 (2019-11-14)
The conserved hypoxia inducible factor 1 α (HIF1α) injury-response pro-survival pathway has recently been implicated in early beta cell dysfunction but slow beta cell loss in type 2 diabetes. We hypothesised that the unexplained prolonged prediabetes phase in type 1
Clinical use of interferon?γ.
Miller C H, et al.
Annals of the New York Academy of Sciences, 1182(1), 69-79 (2009)
The IFNγ receptor: a paradigm for cytokine receptor signaling.
Bach E A, et al.
Annual Review of Immunology, 15(1), 563-591 (1997)
Class II cytokine receptors and their ligands: key antiviral and inflammatory modulators.
Renauld J C.
Nature Reviews: Immunology, 3(8), 667-667 (2003)
Sarah E Nystrom et al.
JCI insight, 7(11) (2022-04-27)
COVID-19 infection causes collapse of glomerular capillaries and loss of podocytes, culminating in a severe kidney disease called COVID-19-associated nephropathy (COVAN). The underlying mechanism of COVAN is unknown. We hypothesized that cytokines induced by COVID-19 trigger expression of pathogenic APOL1
Expression and reconstitution of a biologically active mouse interferon gamma receptor in hamster cells. Chromosomal location of an accessory factor.
Hibino Y, et al.
The Journal of Biological Chemistry, 266(11), 6948-6951 (1991)
In vitro and in vivo cytotoxic effect of AntiGan against tumor cells.
Lombardi V R, et al.
Experimental and Therapeutic Medicine, 15(3), 2547-2556 (2018)
Alexandra C Title et al.
Frontiers in endocrinology, 13, 854094-854094 (2022-07-22)
Restoration of β-cell mass through the induction of proliferation represents an attractive therapeutic approach for the treatment of diabetes. However, intact and dispersed primary islets suffer from rapidly deteriorating viability and function ex vivo, posing a significant challenge for their
Stephan Sachs et al.
Nature metabolism, 2(2), 192-209 (2020-07-23)
Dedifferentiation of insulin-secreting β cells in the islets of Langerhans has been proposed to be a major mechanism of β-cell dysfunction. Whether dedifferentiated β cells can be targeted by pharmacological intervention for diabetes remission, and ways in which this could
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