Sp6 regulation of &lt;i&gt;Rock1 &lt;/i&gt;promoter activity in dental epithelial cells

Yanuaryska, Ryna Dwi; Miyoshi, Keiko; Adiningrat, Arya; Horiguchi, Taigo; Tanimura, Ayako; Hagita, Hiroko; Noma, Takafumi

doi:10.2152/jmi.61.306

Cited by 6 publications

(8 citation statements)

References 25 publications

(30 reference statements)

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“…To reveal the mechanism of dysregulated ROCK1 transcription, we focused on ROCK1‐associated transcription factors. Previous studies demonstrated that transcription factors SP1 and SP6 were involved in ROCK1 gene transcription (Citron, Dennis, Zeitlin, & Echeverria, ; Yanuaryska et al, ; Zhang et al, ; Figure B). Therefore, we investigated the role of SP1 and SP6 in AD and their regulation of ROCK1 expression.…”

Section: Resultsmentioning

confidence: 84%

Rho‐associated coiled‐coil kinase 1 activation mediates amyloid precursor protein site‐specific Ser655 phosphorylation and triggers amyloid pathology

Ren

Zhang

et al. 2019

Aging Cell

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Rho‐associated coiled‐coil kinase 1 (ROCK1) is proposed to be implicated in Aβ suppression; however, the role for ROCK1 in amyloidogenic metabolism of amyloid precursor protein (APP) to produce Aβ was unknown. In the present study, we showed that ROCK1 kinase activity and its APP binding were enhanced in AD brain, resulting in increased β‐secretase cleavage of APP. Furthermore, we firstly confirmed that APP served as a substrate for ROCK1 and its major phosphorylation site was located at Ser655. The increased level of APP Ser655 phosphorylation was observed in the brain of APP/PS1 mice and AD patients compared to controls. Moreover, blockade of APP Ser655 phosphorylation, or inhibition of ROCK1 activity with either shRNA knockdown or Y‐27632, ameliorated amyloid pathology and improved learning and memory in APP/PS1 mice. These findings suggest that activated ROCK1 targets APP Ser655 phosphorylation, which promotes amyloid processing and pathology. Inhibition of ROCK1 could be a potential therapeutic approach for AD.

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Section: Resultsmentioning

confidence: 84%

Rho‐associated coiled‐coil kinase 1 activation mediates amyloid precursor protein site‐specific Ser655 phosphorylation and triggers amyloid pathology

Ren

Zhang

et al. 2019

Aging Cell

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“…These results suggested that defective SP6 protein due to Sp6 mutation could alter the activity of the transcriptional machinery or the unit for cell type‐specific gene expression in ARE cells. To further investigate the underlying molecular mechanisms, we then focused on the expression patterns of Fst, Amtn , and Rock1, because we demonstrated previously that SP6 positively regulated the expression of both Amtn (data not shown) and Rock1 (Yanuaryska et al , ) and negatively regulated the expression of Fst (Ruspita et al , ). Because two ARE clones, ARE‐B6 and ARE‐B30, showed the expression patterns consistent with our previous findings, we chose ARE‐B6 and ARE‐B30 as the representative clones which maintain the effects of Sp6 mutation ( SP6‐AMI ).…”

Section: Resultsmentioning

confidence: 99%

“…Among the ARE clones, ARE-B6 and ARE-B30 showed higher Fst mRNA expression and lower Rock1 mRNA expression than the control G5 cells. Previously, we reported that SP6 could regulate both the underexpression of Fst and the upregulation of Rock1 (Ruspita et al, 2008;Yanuaryska et al, 2014), so these newly identified gene expression profiles might reflect the defective SP6 activity in ARE-B6 and ARE-B30 clones. Therefore, we hypothesized that ARE-B6 and ARE-B30 clones represented good phenocopies for further analysis of the molecular basis for AI.…”

Section: Oral Diseasesmentioning

confidence: 89%

“…We further confirmed in vitro that BMP2 and wingless‐type MMTV integration site family member (Wnt) were the positive regulators of Sp6 expression (Wahyudi et al , ), while chicken ovalbumin upstream promoter transcription factor‐interacting protein 2 (Ctip2) was a negative regulator (Adiningrat et al , ). Furthermore, we found that rho‐associated protein kinase 1 (ROCK1) was positively regulated by SP6 in dental epithelium‐derived cells (Yanuaryska et al , ). It suggests that SP6 is involved in reorganization of the actin cytoskeleton and that it mediates ameloblast differentiation by regulating cell polarity, proliferation, and cell–cell adhesion.…”

Section: Introductionmentioning

confidence: 99%

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Isolation and characterization of dental epithelial cells derived from amelogenesis imperfecta rat

et al. 2016

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“…It always works through binding to the promoter region of its target genes [ 16 , 17 ], and can activate or repress the transcription in response to physiological and pathological stimuli [ 18 ]. The promoter activity of rat ROCK1 gene is reduced by Sp1, whereas it is enhanced by Sp6 in dental epithelial cells [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Transcription Factor Sp1 Promotes the Expression of Porcine ROCK1 Gene

Feng

Zhan

Huang

et al. 2016

IJMS

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Rho-associated, coiled-coil containing protein kinase 1 (ROCK1) gene plays a crucial role in maintaining genomic stability, tumorigenesis and myogenesis. However, little is known about the regulatory elements governing the transcription of porcine ROCK1 gene. In the current study, the transcription start site (TSS) was identified by 5’-RACE, and was found to differ from the predicted one. The region in ROCK1 promoter which is critical for promoter activity was investigated via progressive deletions. Site-directed mutagenesis indicated that the region from −604 to −554 bp contains responsive elements for Sp1. Subsequent experiments showed that ROCK1 promoter activity is enhanced by Sp1 in a dose-dependent manner, whereas treatment with specific siRNA repressed ROCK1 promoter activity. Electrophoretic mobility shift assay (EMSA), DNA pull down and chromatin immunoprecipitation (ChIP) assays revealed Sp1 can bind to this region. qRT-PCR and Western blotting research followed by overexpression or inhibition of Sp1 indicate that Sp1 can affect endogenous ROCK1 expression at both mRNA and protein levels. Overexpression of Sp1 can promote the expression of myogenic differentiation 1(MyoD), myogenin (MyoG), myosin heavy chain (MyHC). Taken together, we conclude that Sp1 positively regulates ROCK1 transcription by directly binding to the ROCK1 promoter region (from −604 to −532 bp) and may affect the process of myogenesis.

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Sp6 regulation of <i>Rock1 </i>promoter activity in dental epithelial cells

Cited by 6 publications

References 25 publications

Rho‐associated coiled‐coil kinase 1 activation mediates amyloid precursor protein site‐specific Ser655 phosphorylation and triggers amyloid pathology

Rho‐associated coiled‐coil kinase 1 activation mediates amyloid precursor protein site‐specific Ser655 phosphorylation and triggers amyloid pathology

Isolation and characterization of dental epithelial cells derived from amelogenesis imperfecta rat

Transcription Factor Sp1 Promotes the Expression of Porcine ROCK1 Gene

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