TMEM174

Last update 08 May 2025

Basic Info

Synonyms

FLJ31268, MGC13034, TMEM174

+ [1]

Introduction

Regulator of plasma phosphate homeostasis. Decreases serum inorganic phosphate (Pi) uptake by regulating the sodium-phosphate cotransporter SLC34A1 trafficking by PTH and FGF23 in the kidney.

100 Clinical Results associated with TMEM174

100 Translational Medicine associated with TMEM174

0 Patents (Medical) associated with TMEM174

Literatures (Medical) associated with TMEM174

01 Aug 2022·Journal of the American Society of NephrologyQ1 · MEDICINE

Targeted Disruption of a Proximal Tubule–Specific TMEM174 Gene in Mice Causes Hyperphosphatemia and Vascular Calcification

Q1 · MEDICINE

Article

Author: Blaine, Judith ; Keenan, Audrey L ; Miyazaki-Anzai, Shinobu ; Miyazaki, Makoto ; Keenan, Audrey L.

Significance StatementHyperphosphatemia is a major complication in the later stages of CKD, causing vascular calcification. We have identified 54 kidney-enriched genes, 19 of which are expressed in renal primary proximal tubule cells. One of the proximal tubule–specific genes, TMEM174, interacted with NPT2A, and its knockdown attenuated the reduction of NPT2A protein by fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH) treatments in proximal tubule cells. TMEM174 knockout mice had significantly increased levels of serum phosphate, FGF23, and PTH, resulting in vascular calcification.BackgroundThe proximal tubules play a critical role in phosphate (Pi) homeostasis by reabsorbing Pi via sodium-dependent Pi cotransporters. NPT2A is a major proximal-specific Pi cotransporter, whose expression is regulated by circulating hormones, such as parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23). In this study, we aimed to find a novel regulator in Pi homeostasis.MethodsUsing RNA-seq and RT-qPCR analysis, we identified proximal tubule cell–enriched genes. We next used RNAi screening of the identified proximal tubular cell–enriched genes to identify a novel proximal tubule–specific gene that contributes to FGF23- and PTH-mediated inhibition of Pi uptake and NPT2 reduction. We created mice lacking this novel regulator of Pi homeostasis to examine whether the novel regulator contributes to Pi homeostasis in vivo.ResultsWe identified 54 kidney-enriched genes, 19 of which are expressed in renal primary proximal tubule cells. One of the proximal tubule–specific genes, TMEM174, interacted with NPT2A, and its knockdown blocked the reduction of NPT2A protein by FGF23 and PTH treatments in human and opossum proximal tubule cells. TMEM174 KO mice had significantly increased levels of serum Pi, FGF23, and PTH, resulting in vascular calcification.ConclusionsTMEM174 is a novel regulator of Pi homeostasis that interacts with NPT2A.

01 Oct 2014·Oncology LettersQ4 · MEDICINE

Analysis of TMEM174 gene expression in various renal cancer types by RNA in situ hybridization

Q4 · MEDICINE

Article

Author: Luo, Mengmeng ; Hu, Fen ; Gou, Lixia ; Zhang, Xiujun ; Meng, Lijun

Transmembrane protein 174 (TMEM174) mRNA is easily detectable in human kidney tissues and activates AP-1 and promotes 293T cell proliferation. In the present study, RNA in situ hybridization was used to detect TMEM174 gene expression in various malignant renal cancer and normal renal tissues. The results showed that TMEM174 exhibits differential expression in renal tissues, with a high positive rate of expression in squamous cell carcinoma with necrosis, papillary renal cell carcinoma and transitional cell carcinoma, and a low positive rate of expression in clear cell carcinoma, interstitial nephritis, undifferentiated carcinoma, retroperitoneal metastatic clear cell carcinoma, adrenal gland metastatic clear cell carcinoma, pelvic cavity metastatic chromophobe carcinoma, severe atypical hyperplasia of transitional epithelium and hyperplasia. Extremely weak expression was exhibited in collecting duct carcinoma, Wilms' tumor, chronic pyelonephritis, acute pyelonephritis, cancer adjacent normal renal tissue and normal renal tissue. In conclusion, the TMEM174 gene exhibited high expression levels in certain renal carcinomas, which may indicate that TMEM174 may have a significant role in the development and progression of these renal carcinomas.

01 Nov 2013·Experimental and Therapeutic MedicineQ4 · MEDICINE

Analysis of promoters and CREB/AP-1 binding sites of the human TMEM174 gene

Q4 · MEDICINE

Article

Author: Yanan Meng ; Lixia Gou ; Xiujun Zhang ; Fen Hu

Transmembrane protein 174 (TMEM174) is a type III transmembrane protein with no clear signal peptide. The N and C terminals are located inside the cell. Our previous study demonstrated high expression of TMEM174 in the kidney and its potential involvement in renal cancer based on its capacity to stimulate cell proliferation. However, the mechanism by which TMEM174 promotes proliferation at the transcriptional level remains to be elucidated. In the present study, the TMEM174 promoter region was amplified from whole blood DNA. Six different regions of the regulatory sequences of the TMEM174 promoter region including ~2.5 kb of the upstream region were cloned into the dual luciferase expression vector pGL3-basic. Comparison of the activity of these fragments in dual luciferase reporter assays revealed higher levels of activity for the fragments spanning -186 to +674, -700 to +674, -1,000 to +674 and -2,500 to +1 bp. Lower levels of activity were detected for the fragments spanning -466 to +674 and -890 to +674 bp. The highest activity was detected for the fragment spanning -186 to +674 bp. Electrophoretic mobility shift assay (EMSA) was performed to determine effective transcription factor binding sites. Specific binding of the cyclic-AMP response element binding (CREB) within the TMEM174 gene promoter region was demonstrated, although binding of the activator protein-1 (AP-1) was also detected in this region. In conclusion, these results suggest that the core promoter region of the human TMEM174 gene is located within the region spanning -186 to +674 bp and that the transcription factors CREB and AP-1 are involved in the transcriptional regulation of this gene.

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