Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 7-Day Trial for You or Your Team.

Learn More →

Why Is There No PiT1/SLC20A1 Pathogenic Variants Yet Linked to Primary Familial Brain Calcification?

Why Is There No PiT1/SLC20A1 Pathogenic Variants Yet Linked to Primary Familial Brain Calcification? LETTER TO THE EDITOR Why Is There No PiT1/SLC20A1 Pathogenic Variants Yet Linked to Primary Familial Brain Calcification? 1 2 Eraldo Fonseca dos Santos-Junior and Joao Ricardo Mendes de Oliveira Keizo Asami Laboratory—Federal University of Pernambuco, Recife, Brazil Federal University of Pernambuco, Recife, Brazil (7) To the Editor of this gene for cell maintenance. In addition to that already discussed here, PiT1 is involved in several other functions such We read with interested the article by Couasnay and colleagues as erythropoiesis, increased insulin signaling, decreased hepatic reporting a new role for PiT1 protein, independent of its inor- lipogenesis, and regulation of apoptosis induced by TNFα,asis (1) ganic phosphate (Pi) transport function, in the regulation and approached by Couasnay and colleagues. (1) homeostasis of the endoplasmic reticulum (ER) in chondro- Couasnay and colleagues show that in chondrocytes, PiT1 (1) cytes. The authors showed that PiT1 is necessary for the main- expression is regulated by ATF4, a transcription factor related tenance, differentiation, and survival of chondrocytes in the to the cytoprotection response performed by the ER. In this same growth plate during endochondral ossification. PiT1 protein is work, the authors further suggest that the regulation of PiT1 by encoded by SLC20A1 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Bone and Mineral Research Oxford University Press

Why Is There No PiT1/SLC20A1 Pathogenic Variants Yet Linked to Primary Familial Brain Calcification?

Download PDF
2 pages

Loading next page...
 
/lp/oxford-university-press/why-is-there-no-pit1-slc20a1-pathogenic-variants-yet-linked-to-primary-0YBblEQtBz

References (10)

Publisher
Oxford University Press
Copyright
© 2020 American Society for Bone and Mineral Research
ISSN
0884-0431
eISSN
1523-4681
DOI
10.1002/jbmr.3973
Publisher site
See Article on Publisher Site

Abstract

LETTER TO THE EDITOR Why Is There No PiT1/SLC20A1 Pathogenic Variants Yet Linked to Primary Familial Brain Calcification? 1 2 Eraldo Fonseca dos Santos-Junior and Joao Ricardo Mendes de Oliveira Keizo Asami Laboratory—Federal University of Pernambuco, Recife, Brazil Federal University of Pernambuco, Recife, Brazil (7) To the Editor of this gene for cell maintenance. In addition to that already discussed here, PiT1 is involved in several other functions such We read with interested the article by Couasnay and colleagues as erythropoiesis, increased insulin signaling, decreased hepatic reporting a new role for PiT1 protein, independent of its inor- lipogenesis, and regulation of apoptosis induced by TNFα,asis (1) ganic phosphate (Pi) transport function, in the regulation and approached by Couasnay and colleagues. (1) homeostasis of the endoplasmic reticulum (ER) in chondro- Couasnay and colleagues show that in chondrocytes, PiT1 (1) cytes. The authors showed that PiT1 is necessary for the main- expression is regulated by ATF4, a transcription factor related tenance, differentiation, and survival of chondrocytes in the to the cytoprotection response performed by the ER. In this same growth plate during endochondral ossification. PiT1 protein is work, the authors further suggest that the regulation of PiT1 by encoded by SLC20A1

Journal

Journal of Bone and Mineral Research – Oxford University Press

Published: Feb 11, 2020

There are no references for this article.