SLC37A2

Last update 08 May 2025

Basic Info

Synonyms

FLJ00171, Glucose-6-phosphate exchanger SLC37A2, SLC37A2

+ [3]

Introduction

Inorganic phosphate and glucose-6-phosphate antiporter. May transport cytoplasmic glucose-6-phosphate into the lumen of the endoplasmic reticulum and translocate inorganic phosphate into the opposite direction. Independent of a lumenal glucose-6-phosphatase. May not play a role in homeostatic regulation of blood glucose levels.

100 Clinical Results associated with SLC37A2

100 Translational Medicine associated with SLC37A2

0 Patents (Medical) associated with SLC37A2

Literatures (Medical) associated with SLC37A2

01 Jan 2023·Cancer Medicine

Establishment of a risk model by integrating hypoxia genes in predicting prognosis of esophageal squamous cell carcinoma

Article

Author: Xiao, Wanyi ; Gong, Lei ; Zhang, Hongdian ; Wu, Xianxian ; Sui, Zhilin ; Yu, Zhentao ; Tang, Peng ; Yang, Yueyang ; Zhu, Ningning ; Han, Youming ; Zhao, Gang

AbstractBackgroundEsophageal squamous cell carcinoma (ESCC) has a dismal prognosis, and hypoxia plays a key role in metastasis and proliferation of ESCC. Thus, we aimed to develop a hypoxia‐based gene signature to assist in the treatment decisions and prognosis.MethodsWe performed consensus clustering analysis on samples from GSE53625 dataset from the Gene Expression Omnibus (GEO) database and used weighted gene co‐expression network analysis to filter out candidate modules, which were then intersected with differentially expressed genes from clustered subgroups to obtain hypoxia‐related genes (HRGs). After that, the aforementioned genes were used to construct risk score models and validated in The Cancer Genome Atlas (TCGA) database and Cox regression analysis were used to construct a nomogram. Immunohistochemical was used to detect protein expression levels of relevant genes. Moreover, the relationship between risk scores and tumor microenvironment was explored.ResultsA hypoxia risk model containing six genes (PNPLA1, CARD18, IL‐18, SLC37A2, ADAMTS18, and FAM83C) was constructed by screening key HRGs. Poorer prognosis in the high‐risk group than in the low‐risk group. And Cox regression analysis showed that risk score was an independent prognostic factor. The nomogram based on risk scores could well predict 1‐, 3‐, and 5‐year survival. P53, Wnt, and hypoxia signaling pathways may be some regulatory mechanisms of hypoxia associated with the tumor microenvironment. In addition, we confirmed the high expression of BGN and low expression of IL‐18 in ESCC tissues.ConclusionsOur study determined the prognostic value of a 6‐hypoxia gene signature and a prognostic model, providing potential prognostic predictors and therapeutic targets for ESCC.

01 Sep 2022·Cell Reports

Mast cell regranulation requires a metabolic switch involving mTORC1 and a glucose-6-phosphate transporter

Article

Author: Abraham, Mathew A ; Iskarpatyoti, Jason A ; Miao, Yuxuan ; Abraham, Soman N ; Shi, Jianling ; Rathore, Abhay P S

Mast cells (MCs) are granulated cells implicated in inflammatory disorders because of their capacity to degranulate, releasing prestored proinflammatory mediators. As MCs have the unique capacity to reform granules following degranulation in vitro, their potential to regranulate in vivo is linked to their pathogenesis. It is not known what factors regulate regranulation, let alone if regranulation occurs in vivo. We report that mice can undergo multiple bouts of MC regranulation following successive anaphylactic reactions. mTORC1, a nutrient sensor that activates protein and lipid synthesis, is necessary for regranulation. mTORC1 activity is regulated by a glucose-6-phosphate transporter, Slc37a2, which increases intracellular glucose-6-phosphate and ATP during regranulation, two upstream signals of mTOR. Additionally, Slc37a2 concentrates extracellular metabolites within endosomes, which are trafficked into nascent granules. Thus, the metabolic switch associated with MC regranulation is mediated by the interactions of a cellular metabolic sensor and a transporter of extracellular metabolites into MC granules.

01 Sep 2022·Molecular Biology of the Cell

Preprint Highlight: Sugar transporter Slc37a2 regulates bone metabolism via a dynamic tubular lysosomal network in osteoclasts

Article

Author: Mantegazza, Adriana

Despite the importance of osteoclast secretory lysosomes (SLs) in bone digestion and resorption, the proteins that reside on SLs are undercharacterized. The authors show that SLC37a2, a unique member of the SLC37 family of sugar ER transporters, localizes to osteoclast SLs and SL tubular networks that support bone resorption. SLC37a2-deficient osteoclasts showed impaired SL membrane tubulation and increased SL size and accumulated monosaccharides, reminiscent of lysosomal storage disorders. Mice lacking SLC37a2 had increased bone mass and strength. As SLC transporters quickly become recognized as metabolic hot spots, SLC37a2 is emerging as a new regulator of lysosomal membrane dynamics and a promising therapeutic target for metabolic bone diseases.

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SLC37A2

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