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GADD45B Promotes Glucose-Induced Renal Tubular Epithelial-Mesenchymal Transition and Apoptosis via the p38 MAPK and JNK Signaling Pathways

https://doi.org/10.3389/fphys.2020.01074

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What this work says

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A more tubulocentric view of diabetic kidney disease

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Triptolide preserves glomerular barrier function via the inhibition of p53-mediated increase of GADD45B

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Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9th edition

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Inhibition of c-Src/p38 MAPK pathway ameliorates renal tubular epithelial cells apoptosis in db/db mice

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A Family of Stress-Inducible GADD45-like Proteins Mediate Activation of the Stress-Responsive MTK1/MEKK4 MAPKKK

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Gadd45β mediates the NF-κB suppression of JNK signalling by targeting MKK7/JNKK2

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HRD1 prevents apoptosis in renal tubular epithelial cells by mediating eIF2α ubiquitylation and degradation

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Triptolide attenuates proteinuria and podocyte apoptosis via inhibition of NF-κB/GADD45B

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Gadd45b mediates depressive-like role through DNA demethylation

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Gadd45a and Gadd45b Protect Hematopoietic Cells from UV-induced Apoptosis via Distinct Signaling Pathways, including p38 Activation and JNK Inhibition

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Tribbles 3 Regulates the Fibrosis Cytokine TGF-β1 through ERK1/2-MAPK Signaling Pathway in Diabetic Nephropathy

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GADD45β Loss Ablates Innate Immunosuppression in Cancer

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Pathology of Human Diabetic Nephropathy

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DNA damage is a novel response to sublytic complement C5b-9–induced injury in podocytes

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Gadd45β promotes hepatocyte survival during liver regeneration in mice by modulating JNK signaling

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Podocyte-Selective Deletion of Dicer Induces Proteinuria and Glomerulosclerosis

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Mechanism of Fibrosis in HNF1B-Related Autosomal Dominant Tubulointerstitial Kidney Disease

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Bcl-2–Modifying Factor Induces Renal Proximal Tubular Cell Apoptosis in Diabetic Mice

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Rap1 Ameliorates Renal Tubular Injury in Diabetic Nephropathy

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