TRNAU1AP

Last update 08 May 2025

Basic Info

Synonyms

FLJ20503, SECP43, tRNA selenocysteine 1 associated protein 1

+ [4]

Introduction

Involved in the early steps of selenocysteine biosynthesis and tRNA(Sec) charging to the later steps resulting in the cotranslational incorporation of selenocysteine into selenoproteins. Stabilizes the SECISBP2, EEFSEC and tRNA(Sec) complex. May be involved in the methylation of tRNA(Sec). Enhances efficiency of selenoproteins synthesis (By similarity).

100 Clinical Results associated with TRNAU1AP

100 Translational Medicine associated with TRNAU1AP

0 Patents (Medical) associated with TRNAU1AP

Literatures (Medical) associated with TRNAU1AP

01 Sep 2024·Nature Biotechnology

Large-scale evaluation of the ability of RNA-binding proteins to activate exon inclusion

Article

Author: Jovanovic, Marko ; Boyle, Evan A ; Kwon, Ester J ; Her, Hsuan-Lin ; Jagannatha, Pratibha ; Luo, En-Ching ; Schmok, Jonathan C ; Jain, Manya ; Street, Lena A ; Yeo, Gene W ; Gosztyla, Maya L ; Schafer, Danielle ; Elmsaouri, Sara ; Tankka, Alex T

AbstractRNA-binding proteins (RBPs) modulate alternative splicing outcomes to determine isoform expression and cellular survival. To identify RBPs that directly drive alternative exon inclusion, we developed tethered function luciferase-based splicing reporters that provide rapid, scalable and robust readouts of exon inclusion changes and used these to evaluate 718 human RBPs. We performed enhanced cross-linking immunoprecipitation, RNA sequencing and affinity purification–mass spectrometry to investigate a subset of candidates with no prior association with splicing. Integrative analysis of these assays indicates surprising roles for TRNAU1AP, SCAF8 and RTCA in the modulation of hundreds of endogenous splicing events. We also leveraged our tethering assays and top candidates to identify potent and compact exon inclusion activation domains for splicing modulation applications. Using these identified domains, we engineered programmable fusion proteins that outperform current artificial splicing factors at manipulating inclusion of reporter and endogenous exons. This tethering approach characterizes the ability of RBPs to induce exon inclusion and yields new molecular parts for programmable splicing control.

01 Mar 2022·Biological Trace Element ResearchQ3 · BIOLOGY

Selenium Deficiency Leads to Changes in Renal Fibrosis Marker Proteins and Wnt/β-Catenin Signaling Pathway Components

Q3 · BIOLOGY

Article

Author: Li, Fenglan ; Tao, Jiaqi ; Zhang, Yutong ; Lin, Tingting ; Liu, Guiyan ; Han, Xueqing ; Zhao, Zihui ; Chen, Ying ; Zhang, Yitong ; Li, Hui

Renal fibrosis is the final result of the progression of chronic kidney disease (CKD) to end-stage renal disease (ESRD). Earlier studies confirmed that selenium (Se) displays a close association with kidney diseases. However, the correlation between Se and fibrosis has rarely been explored. Thus, this article mainly aimed to investigate the effect of Se deficiency on renal fibrosis and the Wnt/β-catenin signaling pathway. Twenty BALB/c mice were fed a diet containing 0.02-mg/kg Se (Se-deficient diet) or 0.18-mg/kg Se (standard diet) for 20 weeks. A human glomerular mesangial cell (HMC) cell line was transfected with lentiviral TRNAU1AP-shRNA vector to establish a stable Se deficiency model in vitro. As indicated in this study, the glutathione (GSH) content in the Se-deficient group displayed an obvious decline compared with that in the control group, whereas the content of malondialdehyde (MDA) was obviously elevated. The results of Masson staining showed fibrosis around the renal tubules, and the results of immunohistochemistry showed that the area of positive fibronectin expression increased. In the Se-deficient group, the levels of collagen I, collagen III, matrix metalloproteinase 9 (MMP9), and other fibrosis-related proteins changed significantly in vivo and in vitro. Compared with the control group, the TRNAU1AP-shRNA group showed markedly reduced cell proliferation and migration abilities. Our data indicate that Se deficiency can cause kidney damage and renal fibrosis. Furthermore, the Wnt pathway is critical for the development of tissue and organ fibrosis. The data of this study demonstrated that the expression of Wnt5a, β-catenin, and dishevelled 1 (Dvl-1) was significantly upregulated in the Se-deficient group. Therefore, the Wnt/β-catenin pathway may play an important role in renal fibrosis caused by Se deficiency.

01 Jan 2021·Biological Trace Element ResearchQ3 · BIOLOGY

Selenium Deficiency-Induced Damage and Altered Expression of Mitochondrial Biogenesis Markers in the Kidneys of Mice

Q3 · BIOLOGY

Article

Author: Lin, Tingting ; Zhang, Yitong ; Lai, Hehuan ; Tao, Jiaqi ; Chen, Ying ; Li, Fenglan ; Li, Hui ; Nie, Tingting ; Ge, Tangdong

Previous studies have raised concerns that kidney disease is often closely related to low serum Se levels in patients and that hyposelenemia may increase the vulnerability of patients to complications. However, few studies examining renal injury caused by Se deficiency have been conducted. To determine the effects of a selenium-deficient diet on renal function, a mouse model was fed a selenium-deficient diet (0.02 mg Se/kg) for 20 weeks. Meanwhile, mice in the control group (selenium-adequate) were fed a standard diet (0.18 mg Se/kg). The cellular models were established by lentiviral Trnau1ap-shRNA vectors transfected into mouse podocyte (MPC5) and mouse renal tubular epithelial (TCMK1) cell lines. Significant increases in serum creatinine levels and urinary protein/creatinine ratios were accompanied by increased MDA content in the Se-deficient group compared to the control group. The morphological observations of tissues showed widespread inflammation and ultrastructural changes in the Se-deficient group, such as swollen mitochondria and extensive podocyte fusion and renal tubular microvilli shedding. In addition, the expression of COXIV and cytochrome c was significantly downregulated in the Se-deficient group. Importantly, the mRNA levels of silent mating type information regulation 2 homolog 1 (SIRT1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and the protein levels of SIRT1 were increased in the Se-deficient group compared with the normal control group. Our data indicate that Se deficiency induces renal injury in mice. The elevated oxidative stress caused by Se deficiency may result in mitochondrial damage, which might affect renal function. Moreover, the SIRT1/PGC1α axis likely plays an important role in the compensatory mechanism of mitochondrial dysfunction.

Analysis

Perform a panoramic analysis of this field.

view full example data

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

TRNAU1AP

Basic Info

Related

Analysis