TESC

Last update 23 Jan 2025

Basic Info

Synonyms

Calcineurin B homologous protein 3, CHP3, FLJ20607

+ [3]

Introduction

Functions as an integral cofactor in cell pH regulation by controlling plasma membrane-type Na(+)/H(+) exchange activity. Promotes the maturation, transport, cell surface stability and exchange activity of SLC9A1/NHE1 at the plasma membrane. Promotes the induction of hematopoietic stem cell differentiation toward megakaryocytic lineage. Essential for the coupling of ERK cascade activation with the expression of ETS family genes in megakaryocytic differentiation. Also involved in granulocytic differentiation in a ERK-dependent manner. Inhibits the phosphatase activity of calcineurin.

100 Clinical Results associated with TESC

100 Translational Medicine associated with TESC

0 Patents (Medical) associated with TESC

Literatures (Medical) associated with TESC

01 Jan 2025·Gene

TESC overexpression mitigates amyloid-β-induced hippocampal atrophy and memory decline

Article

Author: Xu, Jiayuan ; Qi, Jinbo ; Wang, Ping ; Tang, Jie ; Tian, Chunxiao ; Yu, Chunshui ; Dou, Yan ; Xia, Xianyou ; Suo, Xinjun ; Liu, Nana ; Shen, Hui ; Fu, Jilian ; Qin, Wen

BACKGROUND AND OBJECTIVESGenome-wide association studies (GWASs) have identified numerous candidate genes for human brain-imaging phenotypes; however, the biological relevance of many of these genes remains unconfirmed. This study aimed to investigate the causal relationships among tescalcin (TESC) (a GWAS-indicated gene), hippocampal volume, Alzheimer's disease (AD), and the underlying biological mechanisms.METHODSHuman transcriptional data were analyzed to confirm relative TESC expression in the hippocampus. In cell experiments, RNA-seq analysis was used to identify the potential biological pathways for TESC overexpression, and immunofluorescence imaging and cell viability assays were used to evaluate the effect of TESC overexpression on neuronal structure and survival. In animal experiments, the effects of TESC overexpression on hippocampal volume and cognitive function in normal mice and amyloid-β (Aβ)-induced AD mice were investigated by 9.4 T magnetic resonance imaging and behavioral tests. Underlying mechanisms were further assessed via western blotting and electrophysiological recordings.RESULTSHuman transcriptional data demonstrated that TESC is primarily expressed in the hippocampus and neurons. TESC overexpression enhanced the viability of HT22 cells and reduced Aβ-induced cell death. In mouse models, Tesc-overexpressing mice revealed increased hippocampal volume, likely owing to enhanced cell viability and long-term potentiation (LTP), and reducing apoptotic- and oxidation-induced hippocampal damage. TESC overexpression could significantly mitigate Aβ-induced hippocampal atrophy and memory impairment, potentially by reducing Aβ-induced neuronal apoptosis and LTP weakening.CONCLUSIONThis study exemplifies the translation of GWAS findings into actionable biological knowledge and suggests that upregulation of TESC may offer a promising therapeutic strategy for AD.

12 Mar 2024·Clinical and Experimental Immunology

Gene expression analysis revealed downregulation of complement receptor 1 in clonal B cells in cold agglutinin disease

Article

Author: Berentsen, Sigbjørn ; Munthe, Ludvig A ; Tierens, Anne ; Trøen, Gunhild ; Østlie, Ingunn ; Małecki, Jędrzej ; Delabie, Jan ; Tjønnfjord, Geir E ; Małecka, Agnieszka

AbstractCold agglutinin disease (CAD) is a rare B-cell lymphoproliferative disorder of the bone marrow, manifested by autoimmune hemolytic anemia caused by binding of monoclonal IgM autoantibodies to the I antigen. Underlying genetic changes have previously been reported, but their impact on gene expression profile has been unknown. Here, we define differentially expressed genes in CAD B cells. To unravel downstream alteration in cellular pathways, gene expression by RNA sequencing was undertaken. Clonal B-cell samples from 12 CAD patients and IgM-expressing memory B cells from 4 healthy individuals were analyzed. Differential expression analysis and filtering resulted in 93 genes with significant differential expression. Top upregulated genes included SLC4A1, SPTA1, YBX3, TESC, HBD, AHSP, TRAF1, HBA2, RHAG, CA1, SPTB, IL10, UBASH3B, ALAS2, HBA1, CRYM, RGCC, KANK2, and IGHV4-34. They were upregulated at least 8-fold, while complement receptor 1 (CR1/CD35) was downregulated 11-fold in clonal CAD B cells compared to control B cells. Flow cytometry analyses further confirmed reduced CR1 (CD35) protein expression by clonal CAD IgM+ B cells compared to IgM+ memory B cells in controls. CR1 (CD35) is an important negative regulator of B-cell activation and differentiation. Therefore, reduced CR1 (CD35) expression may increase activation, proliferation, and antibody production in CAD-associated clonal B cells.

01 Mar 2024·Environmental Toxicology

Tescalcin modulates bone marrow‐derived mesenchymal stem cells osteogenic differentiation via the Wnt/β‐catenin signaling pathway

Article

Author: Wu, Dong ; Wang, Guangbin ; Piao, Longhuan

AbstractBackgroundBone mesenchymal stem cells (BMSCs) are recognized for their intrinsic capacity for self‐renewal and differentiation into osteoblasts, adipocytes, and chondrocytes, making them pivotal entities within the field of bone research. Tescalcin (TESC) is known to play a role in specific cellular processes related to proliferation and differentiation. However, the precise involvement of TESC in the regulation of BMSCs remains unclear. The present study was designed to verify the functional implications of TESC in BMSCs.MethodsAn adenovirus vector was engineered to downregulate TESC expression, and the Wnt/β‐catenin signaling pathway was activated using BML‐284. The assessment of mRNA was conducted by quantitative real‐time polymerase chain reaction (qRT‐PCR). The assessment of protein expression was conducted by Western blotting and immunofluorescence techniques (IF), respectively. Alkaline phosphatase (ALP) staining and activity assays were performed to verify ALP changes, while Alizarin Red S (ARS) staining and quantitative analysis were employed to assess mineralization capacity.ResultsInitially, we observed an upregulation of TESC expression during osteogenic differentiation. Subsequently, TESC knockdown was demonstrated to decrease the osteogenic‐related genes expression and diminish BMSCs mineralization. Concomitantly, we identified the inhibition of Wnt/β‐catenin signaling following the TESC knockdown. Furthermore, the administration of BML‐284 effectively activated the Wnt/β‐catenin pathway, successfully rescuing the compromised TESC‐mediated osteogenic differentiation.ConclusionOur findings indicate that TESC knockdown exerts an inhibitory effect on the osteogenic differentiation of BMSCs through the modulation of the Wnt/β‐catenin signaling pathway. This study unveils a novel target with potential applications for enhancing the regenerative potential of BMSCs in the realm of regenerative medicine.

Analysis

Perform a panoramic analysis of this field.

view full example data

Chat with Hiro

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

TESC

Basic Info

Related

Analysis