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Igfbp4 is required for inguinal fat expansion in female mice but not in male mice. However, gonadal WAT expansion, which is prevented by estrogen during high-fat diet, does not require Igfbp4.
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IGFBP-4 modulates the skeleton in a gender-specific manner, acting as both a cell autonomous and cell non-autonomous factor.
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exerts a negative effect on basal intestinal growth but plays a positive regulatory role in the intestinotropic actions of GLP-2
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IGF-1/IGFbp4 signaling regulated the post-developmental adipose tissue expansion.
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Igfbp2-5 are expressed in distinct and complementary patterns during cochlear development.
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SOX9 is a transcriptional regulator of IGFBP-4 and that SOX9-induced activation of IGFBP-4 may be one of the mechanisms by which SOX9 suppresses cell proliferation and progression of colon cancer.
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findings indicate that the defect in p53 function and the increased proteolysis of IGFBP-4, we had observed, represent two components of the same pathway, which contributes to the oncogenic function of Skp2B
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Inactivation of IGFBP4 diminished the anabolic effects of PAPP-A on bone.
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Targeted expression of a protease-resistant IGFBP-4 mutant in smooth muscle of transgenic mice
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IGFBP-4 is a potential growth inhibitor of lymphoid tissues.
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This study demonstrates that ES of muscle cells in vitro not only directly modulates the gene expression of contractile proteins but also modulates proteins that are part of the IGF regulatory system, in particular IGFBP-4.
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Crystallization, heparin and IGF binding, and osteogenic activity of IGFBP4 in its native conformation
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Overexpression of Hbegf in transgenic mice downregulates Igfbp4.
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provide direct evidence for combinatorial effects of IGFBP-3, -4, and -5 in both metabolism and at least some soft tissues
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IGFBP-4 may have a role in increasing necrosis and apoptosis, but in decreasing mitosis
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Results indicate that IGFBP-4 functions as a local reservoir to optimize IGF-II actions needed for normal embryogenesis, and also establish that IGFBP-4 proteolysis is required to activate most, if not all, IGF-II mediated growth-promoting activity.
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IGFBP-4 is an inhibitor of the canonical Wnt signalling required for cardiogenesis and provides a molecular link between insulin-like growth factor signalling and Wnt signalling
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Data suggest that loss of expression of IGFBPs (IGFBP-3 and IGFBP-4) in tumor cells treated with EGFR tyrosine kinase inhibitors derepresses IGFIR signaling, which in turn mediates resistance to EGFR antagonists.
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SOD1(G93A) mutant transgenic mice as a model of amyotrophic lateral sclerosis (ALS) and immunohistochemical studies to investigate the changes of insulin-like growth factor-binding protein 4 (IGFBP4) in the central nervous system.