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Interferon Regulatory Factor 9 Protects Against Hepatic Insulin Resistance and Steatosis in Male Mice

https://doi.org/10.1002/hep.26368
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35/35 checkable references clean · checked 2026-07-23

Every reference with a DOI in the deposited reference list resolved to a known work in Crossref or DataCite at the dated check, and none carried a retraction, withdrawal, or removal notice.

5 without a DOI — not checked. A reference deposited without a DOI is never matched by title or guessed at; it stays outside the checked set, and this line discloses that.

The 35 checked references that resolve
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Inflammation and Lipid Signaling in the Etiology of Insulin Resistance
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Mechanisms for Insulin Resistance: Common Threads and Missing Links
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Peroxisome Proliferator-Activated Receptor-γ Coactivator 1α (PGC-1α): Transcriptional Coactivator and Metabolic Regulator
resolves10.1007/s00262-009-0804-6
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resolves10.1038/nri1900
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resolves10.1146/annurev.immunol.26.021607.090400
The IRF Family Transcription Factors in Immunity and Oncogenesis
resolves10.1111/j.1349-7006.2007.00720.x
Interferon regulatory factor family of transcription factors and regulation of oncogenesis
resolves10.1007/s00395-012-0326-9
Interferon regulatory factor 3 is a negative regulator of pathological cardiac hypertrophy
resolves10.1084/jem.20060929
A role for IRF3-dependent RXRα repression in hepatotoxicity associated with viral infections
resolves10.1016/S1097-2765(03)00384-8
Crosstalk between LXR and Toll-like Receptor Signaling Mediates Bacterial and Viral Antagonism of Cholesterol Metabolism
resolves10.1016/j.cmet.2007.11.002
Interferon Regulatory Factors Are Transcriptional Regulators of Adipogenesis
resolves10.1016/j.cmet.2011.02.005
Transcriptional Control of Adipose Lipid Handling by IRF4
resolves10.1074/jbc.M212972200
A Hybrid IRF9-STAT2 Protein Recapitulates Interferon-stimulated Gene Expression and Antiviral Response
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Activation of the Transcription Factor ISGF3 by Interferon-gamma
resolves10.1210/en.2012-1911
CARD3 Deficiency Exacerbates Diet-Induced Obesity, Hepatosteatosis, and Insulin Resistance in Male Mice
resolves10.1016/S0962-8924(01)02207-3
Insulin signaling pathways in time and space
resolves10.1152/physrev.00011.2008
AMPK in Health and Disease
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resolves10.1038/ng0892-372
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<b>Regulation of IFN‐α/β genes: evidence for a dual function of the transcription factor complex ISGF3 in the production and action of IFN‐α/β</b>
resolves10.1172/JCI27989
Sorting out the roles of PPAR  in energy metabolism and vascular homeostasis
resolves10.1210/en.2007-0014
Peroxisome Proliferator-Activated Receptor α Protects against Obesity-Induced Hepatic Inflammation
resolves10.1096/fj.09-151340
JNK1 and IKKβ: molecular links between obesity and metabolic dysfunction
resolves10.1038/nm1166
Local and systemic insulin resistance resulting from hepatic activation of IKK-β and NF-κB
resolves10.1038/nm1185
IKK-β links inflammation to obesity-induced insulin resistance
resolves10.1038/nature01137
A central role for JNK in obesity and insulin resistance
resolves10.1172/JCI113046
Tumor necrosis factor-alpha stimulates hepatic lipogenesis in the rat in vivo.
resolves10.1016/j.jhep.2009.03.008
Kupffer cells in non-alcoholic fatty liver disease: The emerging view
The 5 references without a DOI — listed, not checked
no DOI — not checkedEndoplasmic reticulum stress and the development of diabetes: a review.
no DOI — not checkedHepatic overexpression of SIRT1 in mice attenuates endoplasmic reticulum stress and insulin resistance in the liver.
no DOI — not checkedPPARalphanull mice are protected from highfat dietinduced insulin resistance.
no DOI — not checkedPGC1 promotes insulin resistance in liver through PPARalphadependent induction of TRB3.
no DOI — not checkedSearch for mediators of the lipogenic effects of tumor necrosis factor: potential role for interleukin 6.
What this badge says. CiteStamped means the CHECKABLE references of this work were clean at the dated check: each resolved to a known work in a public registry, and none carried a retraction notice at that time. It says nothing about the quality, findings, or importance of the work itself, and nothing about references deposited without a DOI.

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