scholarly journals Role of phosphatase of regenerating liver 1 (PRL1) in spermatogenesis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yunpeng Bai ◽  
Hong-Ming Zhou ◽  
Lujuan Zhang ◽  
Yuanshu Dong ◽  
Qi Zeng ◽  
...  
Keyword(s):  
Regenerating Liver ◽  
Phosphatase Of Regenerating Liver

scholarly journals A novel role of PRL in regulating epithelial cell density by inducing apoptosis at confluence

2021 ◽  
Author(s):  
Sweksha Lohani ◽  
Yosuke Funato ◽  
Yuki Akieda ◽  
Kiyohito Mizutani ◽  
Yoshimi Takai ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Density ◽  
Mdck Cells ◽  
Zebrafish Embryos ◽  
Developmental Defect ◽  
Convergent Extension ◽  
Regenerating Liver ◽  
Phosphatase Of Regenerating Liver ◽  
Multicellular Organisms

Maintaining proper epithelial cell density is essential for the survival of multicellular organisms. While regulation of cell density through apoptosis is well known, its mechanistic details remain elusive. Here, we report the involvement of membrane-anchored phosphatase of regenerating liver (PRL), originally known for its role in cancer malignancy, in this process. In epithelial MDCK cells, upon confluence, doxycycline-induced expression of PRL upregulated apoptosis, reducing the cell density. This could be circumvented by artificially reducing the cell density via stretching the cell-seeded silicon chamber. Moreover, siRNA-mediated knockdown of endogenous PRL blocked apoptosis, leading to greater cell density. Mechanistically, PRL promoted apoptosis by upregulating the translation of E-cadherin and activating TGF-β pathway. Morpholino-mediated inhibition of PRL expression in zebrafish embryos caused developmental defect with reduced apoptosis and increased epithelial cell density during convergent extension. This study revealed a novel role of PRL in regulating density-dependent apoptosis in vertebrate epithelium.

scholarly journals A Novel Neuroprotective Role of Phosphatase of Regenerating Liver-1 against CO2 Stimulation in Drosophila

iScience ◽  
2019 ◽  
Vol 19 ◽  
pp. 291-302 ◽  
Author(s):  
Pengfei Guo ◽  
Xiao Xu ◽  
Fang Wang ◽  
Xin Yuan ◽  
Yinqi Tu ◽  
...  
Keyword(s):  
Regenerating Liver ◽  
Phosphatase Of Regenerating Liver

scholarly journals Neuroprotective role of Phosphatase of Regenerating Liver-1 against CO2 stimulation in Drosophila

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S89
Author(s):  
Yongmei Xi ◽  
Pengfei Guo ◽  
Xiao Xu ◽  
Xiaohang Yang
Keyword(s):  
Regenerating Liver ◽  
Phosphatase Of Regenerating Liver

The essential role of FKBP38 in regulating phosphatase of regenerating liver 3 (PRL-3) protein stability

2011 ◽  
Vol 406 (2) ◽  
pp. 305-309 ◽  
Author(s):  
Myung-Suk Choi ◽  
Sang-Hyun Min ◽  
Haiyoung Jung ◽  
Ju Dong Lee ◽  
Tae Ho Lee ◽  
...  
Keyword(s):  
Protein Stability ◽  
Essential Role ◽  
Regenerating Liver ◽  
Phosphatase Of Regenerating Liver

Defining the role of the phosphatase of regenerating liver enzymes in the immune system

2015 ◽  
Vol 43 (9) ◽  
pp. S66
Author(s):  
Teri Hatzihristidis ◽  
Noriko Uetani ◽  
Serge Hardy ◽  
Jacinthe Sirois ◽  
Michel L. Tremblay
Keyword(s):  
Immune System ◽  
Liver Enzymes ◽  
Regenerating Liver ◽  
Phosphatase Of Regenerating Liver

Phosphatase of regenerating liver sensitizes MET to functional activation by hepatocyte growth factor

2019 ◽  
Vol 476 (10) ◽  
pp. 1419-1431
Author(s):  
Takuya Kojima ◽  
Yosuke Funato ◽  
Hiroaki Miki
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Hepatocyte Growth Factor ◽  
Cellular Level ◽  
Malignant Progression ◽  
Regenerating Liver ◽  
Downstream Signaling ◽  
Phosphatase Of Regenerating Liver ◽  
Hepatocyte Growth

Abstract Phosphatase of regenerating liver (PRL) is overexpressed in metastatic cancers and actively drives their malignant progression. Many studies on cultured cancer cells have implied PRL overexpression as a stimulant for cellular signaling involved in cell proliferation. However, its role in the tightly adhered and polarized epithelial cells remains largely uncharacterized. In this study, we show that inducible expression of PRL in MDCK normal epithelial cells sensitized MET, the receptor for hepatocyte growth factor (HGF), to functional activation by HGF. We found that PRL expression amplified tyrosine phosphorylation levels of various proteins, among which MET was identified to be the most abundant. This phosphorylation occurred selectively at Y1234/1235 in the activation loop of MET, whereas phosphorylation of Y1349 in the effector-binding site, which is directly involved in downstream signaling, was almost undetectable. Consistently, PRL overexpression by itself did not cause observable alterations at the cellular level. However, when cells were stimulated with HGF, phosphorylation of Y1349 was much more strongly induced in PRL-expressing cells than in control cells. This resulted in robust cell scattering and tubulogenesis, even with low levels of HGF. Collectively, these results demonstrate a unique role of PRL in regulating MET function, which is known to be crucial for remodeling of epithelial tissues and malignant progression of cancers.

scholarly journals Regulatory mechanisms of phosphatase of regenerating liver (PRL)-3

2016 ◽  
Vol 44 (5) ◽  
pp. 1305-1312 ◽  
Author(s):  
Teresa Rubio ◽  
Maja Köhn
Keyword(s):  
Drug Development ◽  
Posttranslational Modifications ◽  
Human Cancer ◽  
Regulatory Mechanisms ◽  
Therapeutic Drug ◽  
Regenerating Liver ◽  
Cancer Types ◽  
Tumor Metastases ◽  
Phosphatase Of Regenerating Liver ◽  
Incomplete Picture

The phosphatase of regenerating liver (PRL)-3 is overexpressed in many human cancer types and tumor metastases when compared with healthy tissues. Different pathways and mechanisms have been suggested to modulate PRL-3 expression levels and activity, giving some valuable insights but still leaving an incomplete picture. Investigating these mechanisms could provide new targets for therapeutic drug development. Here, we present an updated overview and summarize recent findings concerning the different PRL-3 expression regulatory mechanisms and posttranslational modifications suggested to modulate the activity, localization, or stability of this phosphatase.

Sign in / Sign up

Export Citation Format

Share Document