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| http://dx.doi.org/10.1002/mdc3.12250 | DOI Listing |
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An Intrabody against B-Cell Receptor-Associated Protein 31 (BAP31) Suppresses the Glycosylation of the Epithelial Cell-Adhesion Molecule (EpCAM) via Affecting the Formation of the Sec61-Translocon-Associated Protein (TRAP) Complex.
Int J Mol Sci
September 2023
College of Life Science and Health, Northeastern University, 195 Chuangxin Road, Hunnan District, Shenyang 110819, China.
The epithelial cell-adhesion molecule (EpCAM) is hyperglycosylated in carcinoma tissue and the oncogenic function of EpCAM primarily depends on the degree of glycosylation. Inhibiting EpCAM glycosylation is expected to have an inhibitory effect on cancer. We analyzed the relationship of BAP31 with 84 kinds of tumor-associated antigens and found that BAP31 is positively correlated with the protein level of EpCAM.
View Article and Find Full Text PDFA novel mitochondria-related gene signature in esophageal carcinoma: prognostic, immune, and therapeutic features.
Funct Integr Genomics
March 2023
Department of Medical Cellular Biology and Genetics, School of Basic Medical Science, Shanxi Medical University, Shanxi, 030001, Taiyuan, China.
Esophageal carcinoma (ESCA) is a common and lethal malignant tumor worldwide. The mitochondrial biomarkers were useful in finding significant prognostic gene modules associated with ESCA owing to the role of mitochondria in tumorigenesis and progression. In the present work, we obtained the transcriptome expression profiles and corresponding clinical information of ESCA from The Cancer Genome Atlas (TCGA) database.
View Article and Find Full Text PDFA Novel Ferroptosis-Related Gene Signature to Predict Prognosis of Esophageal Carcinoma.
J Oncol
July 2022
Department of Radiotherapy, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou 213003, Jiangsu Province, China.
Objective: This study aimed to develop a novel ferroptosis-related gene-based prognostic signature for esophageal carcinoma (ESCA).
Methods: The TCGA-ESCA gene expression profiles and corresponding clinical data were downloaded from the TCGA database. Ferroptosis-related genes were identified from the literature and public databases, which were intersected with the differentially expressed genes between ESCA and normal samples.
BAP31: Physiological functions and roles in disease.
Biochimie
July 2021
Department of Molecular Biology and Genetics - DANDRITE, Aarhus University, Gustav Wieds Vej 10, DK-8000 Aarhus C, Denmark. Electronic address:
B-cell receptor-associated protein 31 (BAP31 or BCAP31) is a ubiquitously expressed transmembrane protein found mainly in the endoplasmic reticulum (ER), including in mitochondria-associated membranes (MAMs). It acts as a broad-specificity membrane protein chaperone and quality control factor, which can promote different fates for its clients, including ER retention, ER export, ER-associated degradation (ERAD), or evasion of degradation, and it also acts as a MAM tetherer and regulatory protein. It is involved in several cellular processes - it supports ER and mitochondrial homeostasis, promotes proliferation and migration, plays several roles in metabolism and the immune system, and regulates autophagy and apoptosis.
View Article and Find Full Text PDFFurther delineation of BCAP31-linked intellectual disability: description of 17 new families with LoF and missense variants.
Eur J Hum Genet
September 2021
Département de génétique médicale, AP-HM, Hôpital d'enfants La Timone, Marseille, France.
Article Synopsis
- The BCAP31 gene at Xq28 encodes BAP31, which is involved in transporting proteins from the endoplasmic reticulum to the Golgi apparatus, with mutations linked to severe neurological disorders in males.
- Pathogenic variants result in a spectrum of symptoms, including profound intellectual disability, dystonia, deafness, and a syndrome called deafness, dystonia, and cerebral hypomyelination (DDCH), with females often being asymptomatic or only mildly affected.
- The study identifies 17 new families with BCAP31-related conditions, confirming that males with loss-of-function variants have a more severe phenotype, while females can exhibit a range of neurological symptoms, and suggests additional complications like elevated liver enzymes in male
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