NIPSNAP2

Last update 08 May 2025

Basic Info

Synonyms

GBAS, Glioblastoma-amplified sequence, nipsnap homolog 2

+ [2]

Introduction

Protein involved in mitophagy by facilitating recruitment of the autophagy machinery required for clearance of damaged mitochondria (PubMed:30982665). Accumulates on the mitochondria surface in response to mitochondrial depolarization and acts as a 'eat me' signal by recruiting proteins involved in selective autophagy, such as autophagy receptors (CALCOCO2/NDP52, NBR1, SQSTM1/p62, TAX1BP1 and WDFY3/ALFY) and ATG8 family proteins (MAP1LC3A, MAP1LC3B, MAP1LC3C, GABARAP, GABARAPL1 and GABARAPL2) (PubMed:30982665).

100 Clinical Results associated with NIPSNAP2

100 Translational Medicine associated with NIPSNAP2

0 Patents (Medical) associated with NIPSNAP2

Literatures (Medical) associated with NIPSNAP2

01 Jun 2024·Aging Cell

Autophagy gene expression in skeletal muscle of older individuals is associated with physical performance, muscle volume and mitochondrial function in the study of muscle, mobility and aging (SOMMA)

Article

Author: Huo, Zhiguang ; Hepple, Russell T. ; Barnes, Haley N. ; Santiago‐Fernández, Olaya ; Evans, Daniel S. ; Coen, Paul M. ; Toledo, Frederico G. S. ; Kritchevsky, Stephen B. ; Tranah, Gregory J. ; Cuervo, Ana Maria ; Wu, Kevin ; Esser, Karyn A. ; Zhang, Xiping ; Cawthon, Peggy M. ; Newman, Anne B. ; Wolff, Christopher A. ; Cummings, Steven R.

AbstractAutophagy is essential for proteostasis, energetic balance, and cell defense and is a key pathway in aging. Identifying associations between autophagy gene expression patterns in skeletal muscle and physical performance outcomes would further our knowledge of mechanisms related with proteostasis and healthy aging. Muscle biopsies were obtained from participants in the Study of Muscle, Mobility, and Aging (SOMMA). For 575 participants, RNA was sequenced and expression of 281 genes related to autophagy regulation, mitophagy, and mTOR/upstream pathways was determined. Associations between gene expression and outcomes including mitochondrial respiration in muscle fiber bundles (MAX OXPHOS), physical performance (VO2 peak, 400 m walking speed, and leg power), and thigh muscle volume, were determined using negative binomial regression models. For autophagy, key transcriptional regulators including TFE3 and NFKB‐related genes (RELA, RELB, and NFKB1) were negatively associated with outcomes. On the contrary, regulators of oxidative metabolism that also promote overall autophagy, mitophagy, and pexophagy (PPARGC1A, PPARA, and EPAS1) were positively associated with multiple outcomes. In line with this, several mitophagy, fusion, and fission‐related genes (NIPSNAP2, DNM1L, and OPA1) were also positively associated with outcomes. For mTOR pathway and related genes, expression of WDR59 and WDR24, both subunits of GATOR2 complex (an indirect inhibitor of mTORC1), and PRKAG3, which is a regulatory subunit of AMPK, were negatively correlated with multiple outcomes. Our study identifies autophagy and selective autophagy such as mitophagy gene expression patterns in human skeletal muscle related to physical performance, muscle volume, and mitochondrial function in older persons which may lead to target identification to preserve mobility and independence.

03 Feb 2022·The OncologistQ2 · MEDICINE

GBAS Regulates the Proliferation and Metastasis of Ovarian Cancer Cells by Combining with eEF1A1

Q2 · MEDICINE

Article

Author: Ren, Sujing ; Shi, Guangyue ; Ma, Rong ; Li, Lianwei ; Liu, Shuang ; Zhang, Ruichun ; Ning, Xin ; Meng, Fanling ; Xie, Qin ; Ding, Jing ; Xu, Wei

AbstractBackgroundThe glioblastoma-amplified sequence (GBAS) is a newly identified gene that is amplified in approximately 40% of glioblastomas. This article probes into the expression, prognostic significance, and possible pathways of GBAS in ovarian cancer (OC).MethodImmunohistochemical methods were used to evaluate the expression level of GBAS in OC and its relationship with clinicopathological characteristics and prognosis. Glioblastoma-amplified sequence shRNA was designed to transfect into OC cell lines to silence GBAS expression, then detect the proliferation, apoptosis, and migration ability of the cell. Furthermore, an in vitro tumor formation experiment in mice was constructed to prove the effect of GBAS expression on the growth of OC in vivo. To further study the regulation mechanism of GBAS, we performed co-immunoprecipitation (Co-IP) and shotgun LC-MS mass spectrometry identification.ResultsImmunohistochemistry indicated that GBAS was markedly overexpressed in OC compared with normal ovarian tissue and was associated with lymph node metastasis. Inhibition of GBAS expression can significantly reduce OC cell proliferation, colony formation, promote cell apoptosis, and reduce the ability of cell migration and invasion. In vivo tumor formation experiments showed that the size and weight of tumors in mice after GBAS expression knockdown was significantly smaller. Glioblastoma-amplified sequence may be combined with elongation factor 1 alpha 1 (eEF1A1) to achieve its regulation in OC. Bioinformatics analysis data indicate that GBAS may be a key regulator of mitochondria-associated pathways, therefore controlling cancer progression. MicroRNA-27b, MicroRNA-23a, and MicroRNA-590 may directly targeting GBAS affects the biological behavior of OC cells.ConclusionThe glioblastoma-amplified sequence may regulate the proliferation and metastasis of OC cells by combining with eEF1A1.

01 Jun 2021·Photodiagnosis and Photodynamic TherapyQ3 · MEDICINE

Co-delivery of chitosan nanoparticles of 5-aminolevulinic acid and shGBAS for improving photodynamic therapy efficacy in oral squamous cell carcinomas

Q3 · MEDICINE

Article

Author: Shufang Li ; Xing Wang ; Hongwei Liu

BACKGROUNDThe improvement of gene therapy provides hope for the treatment of cancer. However, malignant tumor is a multifactorial disease, which remains difficult to be cured with a single therapy. Our previous study reported that mitochondrial genes glioblastoma-amplified sequence (GBAS) plays a role in the development and treatment of oral squamous cell carcinoma (OSCC). The current study focused on building a mitochondrial-targeting drug co-delivery system for combined photodynamic therapy (PDT) and gene therapy.METHODS5-aminolevulinic acid (ALA) photosensitizer loaded chitosan (CS) nanoparticles were prepared using ionic crosslinking method, and further synthesized with the GBAS gene plasmid DNA (shGBAS) by electrostatic attraction. We detected the effects of PDT using the co-delivery system (CS-ALA-shGBAS) on cell proliferation and mitochondrial injury by MTT and reactive oxygen species (ROS) assays, respectively. Additionally, a oral cancer Xenograft model of nude mice was built to test its inhibitive effect on the cancerous growth in vivo.RESULTSA novel nanocomposite, CS-ALA-shGBAS, was found to be spherical structures and had good dispersion, stability and hypotoxicity. Gel retardation assay showed that CS-ALA nanoparticle could synthesize shGBAS at and above Nanoparticle/Plasmid ratios of 1/2. Excitingly, the co-delivery system was suitable for transfected cells and displayed a superior mitochondrially targeted killing effect on OSCC in vitro and in vivo.CONCLUSIONOur study provides evidence that the chitosan-based co-delivery system of ALA-induced protoporphyrin IX (PpIX) photosensitizer and GBAS gene may be a novel mode of combined therapy for OSCC.

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