ArticleOncotarget2016
Decreased DACH1 expression in glomerulopathy is associated with disease progression and severity.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Dach1 is essential for maintaining normal mature podocytes.PloS one · 2024Article
- TheViruses · 2023Article
- Effects of a High-Protein Diet on Kidney Injury under Conditions of Non-CKD or CKD in Mice.International journal of molecular sciences · 2023Article
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
- Network-based identification and prioritization of key transcriptional factors of diabetic kidney disease.Computational and structural biotechnology journal · 2023Article
- Sequence-specific recognition of a coding segment of humanRSC advances · 2021Article
- DACH1 protects podocytes from experimental diabetic injury and modulates PTIP-H3K4Me3 activity.The Journal of clinical investigation · 2021Article
- DACH1 as a multifaceted and potentially druggable susceptibility factor for kidney disease.The Journal of clinical investigation · 2021Article
- Transcriptome-wide association analysis identifies DACH1 as a kidney disease risk gene that contributes to fibrosis.The Journal of clinical investigation · 2021Article
- Upregulation of microRNA‑140‑3p mediates dachshund family transcription factor 1 expression in immunoglobulin A nephropathy through cell cycle‑dependent mechanisms.Molecular medicine reports · 2021Article
- Article
- The Plasma Soluble Urokinase Plasminogen Activator Receptor Is Related to Disease Activity of Patients with ANCA-Associated Vasculitis.Mediators of inflammation · 2020Article
- Global polysome analysis of normal and injured podocytes.American journal of physiology. Renal physiology · 2019Article
- The transcription factor Dach1 is essential for podocyte function.Journal of cellular and molecular medicine · 2018Article
- DACH1 antagonizes CXCL8 to repress tumorigenesis of lung adenocarcinoma and improve prognosis.Journal of hematology & oncology · 2018Article
- Differential gene and lncRNA expression in the lower thoracic spinal cord following ischemia/reperfusion-induced acute kidney injury in rats.Oncotarget · 2017Article
- DACH1 suppresses breast cancer as a negative regulator of CD44.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell fate determination factor dachshund1 (DACH1) is a chromosome-associated protein that regulates cellular differentiation throughout development. Recent genome-wide association studies have show that missense mutation in DACH1 leads to hereditary renal hypodysplasia. Renal DACH1 expression can be used to estimate glomerular filtration rate (eGFR). We firstly characterized the function of DACH1 in normal and diseased renal tissue using immunohistochemistry to assess DACH1 in human renal biopsy specimens from 40 immunoglobulin A nephropathy (IgAN) patients, 20 idiopathic membranous nephropathy (IMN) patients, and 15 minimal change disease (MCD) patients. We found that DACH1 expression was decreased in the nephropathy group relative to healthy controls. DACH1 staining in the glomerulus correlated positively with eGFR (r = 0.41, p < 0.001) but negatively with serum creatinine (r = -0.37, p < 0.01). In vitro, DACH1 overexpression in human podocytes or HK2 cells decreased expression of cyclin D1, but increased expression of p21 and p53, which suggested that DACH1 overexpression in human podocytes or HK2 cells increased the G1/S phase or G2/M cell arrest. Together, These findings indicate that DACH1 expression is decreased in glomerulopathy imply a potential role for DACH1 in the this development of human chornic glomerulopathy. These data suggest that DACH1 is a potential a marker of disease progression and severity for glomerular diseases.
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