Retraction: Cholesterol depletion inhibits epidermal growth factor receptor transactivation by angiotensin II in vascular smooth muscle cells. ROLE OF CHOLESTEROL-RICH MICRODOMAINS AND FOCAL ADHESIONS IN ANGIOTENSIN II SIGNALING.

Fukai, Masuko; Hilenski, Lula; Santanam, Nalini; Becker, Peter L.; Ma, Yuxian; Griendling, Kathy K.; Alexander, R. Wayne

doi:10.1074/jbc.a113.105901

Cited by 18 publications

(27 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This possibility is supported by the findings that MMP9-deficient mice exhibit a decrease in UB branching [111]. Since caveolae/lipid rafts are essential for Ang II-induced transactivation of EGF RTK, another possible mechanism facilitating Ang II interactions with EGF/Ret RTKs may involve direct physical interaction between AT 1 R/AT 2 R and RTKs in lipid rafts [112].…”

Section: Activation Of Ret Rtk Signaling By Ang IImentioning

confidence: 82%

Renin–angiotensin system in ureteric bud branching morphogenesis: insights into the mechanisms

Yosypiv

2011

Pediatr Nephrol

View full text Add to dashboard Cite

Branching morphogenesis of the ureteric bud (UB) is a key developmental process that controls organogenesis of the entire metanephros. Notably, aberrant UB branching may result in a spectrum of congenital anomalies of the kidney and urinary tract (CAKUT). Genetic, biochemical and physiological studies have demonstrated that the renin-angiotensin system (RAS), a key regulator of the blood pressure and fluid/electrolyte homeostasis, also plays a critical role in kidney development. All the components of the RAS are expressed in the metanephros. Moreover, mutations in the genes encoding components of the RAS in mice or humans cause diverse types of CAKUT which include renal papillary hypoplasia, hydronephrosis, duplicated collecting system, renal tubular dysgenesis, renal vascular abnormalities, abnormal glomerulogenesis and urinary concentrating defect. Despite widely accepted role of the RAS in metanephric kidney and renal collecting system (ureter, pelvis, calyces and collecting ducts) development, the mechanisms by which an intact RAS exerts its morphogenetic actions are incompletely defined. Emerging evidence indicates that defects in UB branching morphogenesis may be causally linked to the pathogenesis of renal collecting system anomalies observed under conditions of aberrant RAS signaling. This review describes the role of the RAS in UB branching morphogenesis and highlights emerging insights into the cellular and molecular mechanisms whereby RAS regulates this critical morphogenetic process.

show abstract

Section: Activation Of Ret Rtk Signaling By Ang IImentioning

confidence: 82%

Renin–angiotensin system in ureteric bud branching morphogenesis: insights into the mechanisms

Yosypiv

2011

Pediatr Nephrol

View full text Add to dashboard Cite

show abstract

“…Lipid raft formation is regulated by cholesterol content (20,43,44) and facilitates the membrane trafficking of cholesterol-binding proteins (45). The suppression of SQS in prostate cancer has been shown to reduce the level of raft-associated cholesterol, leading to reduced cell proliferation but elevated cell death (21).…”

Section: Discussionmentioning

confidence: 99%

Squalene Synthase Induces Tumor Necrosis Factor Receptor 1 Enrichment in Lipid Rafts to Promote Lung Cancer Metastasis

Yang

Jan

Liu³

et al. 2014

Am J Respir Crit Care Med

View full text Add to dashboard Cite

show abstract

“…Both are known to almost completely abolish the presence of caveolae (47,52). Figure 4A shows that both agents prevented HG-induced RhoA activation.…”

Section: F162 Caveolae Mediate Ros Generation In High Glucosementioning

confidence: 99%

High glucose-induced RhoA activation requires caveolae and PKCβ1-mediated ROS generation

Zhang

Peng

Gao

et al. 2012

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

show abstract

Retraction: Cholesterol depletion inhibits epidermal growth factor receptor transactivation by angiotensin II in vascular smooth muscle cells. ROLE OF CHOLESTEROL-RICH MICRODOMAINS AND FOCAL ADHESIONS IN ANGIOTENSIN II SIGNALING.

Abstract: Committee found evidence of inappropriate image manipulation in Figs. 2A and 3 that caused misrepresentation of the data.

Cited by 18 publications

References 0 publications

Renin–angiotensin system in ureteric bud branching morphogenesis: insights into the mechanisms

Renin–angiotensin system in ureteric bud branching morphogenesis: insights into the mechanisms

Squalene Synthase Induces Tumor Necrosis Factor Receptor 1 Enrichment in Lipid Rafts to Promote Lung Cancer Metastasis

High glucose-induced RhoA activation requires caveolae and PKCβ1-mediated ROS generation

Contact Info

Product

Resources

About