TAZ enhances mammary cell proliferation in 3D culture through transcriptional regulation of IRS1

Rensburg, Helena J. Janse van; Lai, Dehui; Azad, Taha; Hao, Yawei; Yang, Xiaolong

doi:10.1016/j.cellsig.2018.08.012

Cited by 13 publications

(11 citation statements)

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“…Overexpression of TAZ drived stromal cell proliferation, while silencing of TAZ had the opposite effect. Consistently, TAZ might exert proliferative activity in mammary and periodontal ligament stem cells, and stimulate liver regeneration by increasing hepatocyte proliferation 31 – 33 . It is known that cellular proliferation is accompanied by the alteration of cell cycle 34 .…”

Section: Discussionmentioning

confidence: 89%

TAZ as a novel regulator of oxidative damage in decidualization via Nrf2/ARE/Foxo1 pathway

Zheng

Yang

et al. 2021

Exp Mol Med

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TAZ, as a crucial effector of Hippo pathway, is required for spermatogenesis and fertilization, but little is known regarding its physiological function in uterine decidualization. In this study, we showed that TAZ was localized in the decidua, where it promoted stromal cell proliferation followed by accelerated G1/S phase transition via Ccnd3 and Cdk4 and induced the expression or activity of stromal differentiation markers Prl8a2, Prl3c1 and ALP, indicating the importance of TAZ in decidualization. Knockdown of TAZ impeded HB-EGF induction of stromal cell proliferation and differentiation. Under oxidative stress, TAZ protected stromal differentiation against oxidative damage by reducing intracellular ROS and enhancing cellular antioxidant capacity dependent on the Nrf2/ARE/Foxo1 pathway. TAZ strengthened the transcriptional activity of Nrf2 which directly bound to the antioxidant response element (ARE) of Foxo1 promoter region. Additionally, silencing TAZ caused accumulation of intracellular ROS through heightening NOX activity whose blockade by APO reversed the disruption in stromal differentiation. Further analysis revealed that TAZ might restore mitochondrial function, as indicated by the increase in ATP level, mtDNA copy number and mitochondrial membrane potential with the reduction in mitochondrial superoxide. Additionally, TAZ modulated the activities of mitochondrial respiratory chain complexes I and III whose suppression by ROT and AA resulted in the inability of TAZ to defend against oxidative damage to stromal differentiation. Moreover, TAZ prevented stromal cell apoptosis by upregulating Bcl2 expression and inhibiting Casp3 activity and Bax expression. In summary, TAZ might mediate HB-EGF function in uterine decidualization through Ccnd3 and ameliorate oxidative damage to stromal cell differentiation via Nrf2/ARE/Foxo1 pathway.

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Section: Discussionmentioning

confidence: 89%

TAZ as a novel regulator of oxidative damage in decidualization via Nrf2/ARE/Foxo1 pathway

Zheng

Yang

et al. 2021

Exp Mol Med

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“…The activated RTK and signaling proteins form a signaling complex that broadcasts signals along other signaling pathways. It has been shown that PI3-kinase (PI3K), one of the main downstream signaling pathways of RTKs, induces YAP/TAZ nuclear localization through inhibition of LATS activity (Figure 2) [48,49]. Recently, we provided the first evidence that the Hippo pathway effectors TAZ and YAP are critical mediators of PI3K-induced mammary tumorigenesis and synergistically function together with PI3K in transformation of mammary cells [50].…”

Section: Introductionmentioning

confidence: 99%

The Role of YAP and TAZ in Angiogenesis and Vascular Mimicry

Azad

Ghahremani

Yang

2019

Cells

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Angiogenesis, the formation of new blood vessels from pre-existing vasculature, is a physiological process that begins in utero and continues throughout life in both good health and disease. Understanding the underlying mechanism in angiogenesis could uncover a new therapeutic approach in pathological angiogenesis. Since its discovery, the Hippo signaling pathway has emerged as a key player in controlling organ size and tissue homeostasis. Recently, new studies have discovered that Hippo and two of its main effectors, Yes-associated protein (YAP) and its paralog transcription activator with PDZ binding motif (TAZ), play critical roles during angiogenesis. In this review, we summarize the mechanisms by which YAP/TAZ regulate endothelial cell shape, behavior, and function in angiogenesis. We further discuss how YAP/TAZ function as part of developmental and pathological angiogenesis. Finally, we review the role of YAP/TAZ in tumor vascular mimicry and propose directions for future work.

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“…Plasmid encoding SARS-CoV-2 spike pseudotyped lentivirus was kindly provided by Dr. Jesse Bloom (Fred Hutchinson Cancer Research Center, Seattle, WA, USA) and lentivirus was generated as previously described [29] HEK293T cells were seeded in 6 wells plates to 70% confluency and were transfected with 1ug of individual smBiT ACE2 mutant DNA using PolyJet (SignaGen, Frederick, MD, USA) according to manufacturer's protocol. 48 h post-transfection, supernatants of transfected cells were harvested.…”

Section: Lentiviral Pseudovirus Assaymentioning

confidence: 99%

Characterization of Critical Determinants of ACE2–SARS CoV-2 RBD Interaction

Brown

Rezaei

Jamieson

et al. 2021

IJMS

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Despite sequence similarity to SARS-CoV-1, SARS-CoV-2 has demonstrated greater widespread virulence and unique challenges to researchers aiming to study its pathogenicity in humans. The interaction of the viral receptor binding domain (RBD) with its main host cell receptor, angiotensin-converting enzyme 2 (ACE2), has emerged as a critical focal point for the development of anti-viral therapeutics and vaccines. In this study, we selectively identify and characterize the impact of mutating certain amino acid residues in the RBD of SARS-CoV-2 and in ACE2, by utilizing our recently developed NanoBiT technology-based biosensor as well as pseudotyped-virus infectivity assays. Specifically, we examine the mutational effects on RBD-ACE2 binding ability, efficacy of competitive inhibitors, as well as neutralizing antibody activity. We also look at the implications the mutations may have on virus transmissibility, host susceptibility, and the virus transmission path to humans. These critical determinants of virus–host interactions may provide more effective targets for ongoing vaccines, drug development, and potentially pave the way for determining the genetic variation underlying disease severity.

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TAZ enhances mammary cell proliferation in 3D culture through transcriptional regulation of IRS1

Cited by 13 publications

References 50 publications

TAZ as a novel regulator of oxidative damage in decidualization via Nrf2/ARE/Foxo1 pathway

TAZ as a novel regulator of oxidative damage in decidualization via Nrf2/ARE/Foxo1 pathway

The Role of YAP and TAZ in Angiogenesis and Vascular Mimicry

Characterization of Critical Determinants of ACE2–SARS CoV-2 RBD Interaction

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