Ask about this productRelated genes to: TBL2 antibody
- Gene:
- TBL2 NIH gene
- Name:
- transducin beta like 2
- Previous symbol:
- -
- Synonyms:
- WS-betaTRP, WBSCR13, DKFZP43N024
- Chromosome:
- 7q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-14
- Date modifiied:
- 2016-07-27
Related products to: TBL2 antibody
Related articles to: TBL2 antibody
- Glioblastoma (GBM) is the most common primary malignant brain tumor in the central nervous system. The role of autophagy in GBM is highly complex, as it can promote both tumor cell survival and suppression of tumor progression. TBL2 is aberrantly expressed in various cancers and has been closely associated with tumor initiation and progression. This study aims to elucidate the role of TBL2 in GBM. Bioinformatics analysis of The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases were performed to evaluate TBL2 expression. Quantitative real-time PCR (qRT-PCR) and Western blot was used to validate TBL2 expression in GBM cells. The biological functions of TBL2 in GBM progression (including cell proliferation, apoptosis, migration, and invasion) were assessed using siRNA-mediated knockdown of TBL2. Additionally, autophagy regulation was examined to explore the potential mechanisms through which TBL2 influences GBM progression. Our results demonstrated that knockdown of TBL2 significantly inhibited GBM cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while promoting apoptosis. Moreover, TBL2 silencing enhanced autophagy via the AMPK/mTOR signaling pathway. Further investigations revealed that AMPK activation augmented the inhibitory effects of TBL2 silencing on GBM cell migration, invasion, and EMT, and promoted apoptosis. Conversely, inhibition of autophagy with chloroquine attenuated the suppressive effects of TBL2 knockdown on GBM cell proliferation, migration, invasion, and EMT. In conclusion, this study identifies a novel regulatory mechanism through which TBL2 promotes GBM progression by modulating autophagy via the AMPK/mTOR pathway. These findings suggest that TBL2 may represent a potential therapeutic target for GBM. - Source: PubMed
Publication date: 2025/10/14
Wang ShanMeng HangDou XiaKong LingyuWang WenjingHou MengnanYan YanLi BinJin Tianbo - Elucidating the genetic basis of lipid metabolism in children is essential for early intervention in dyslipidemia and cardiovascular diseases. We performed a two-staged genome-wide association study (GWAS; N = 5412) and an independent exome-wide association study (ExWAS; N = 4750) on lipid parameters-HDL, LDL, Triglycerides (TG), Total Cholesterol (TC) in Indian school-going children - the largest single-cohort paediatric lipid study till date. GWAS identified robust associations at established loci, including CETP for HDL; CELSR2, and PSRC1 for LDL and TC, and GCKR, ZNF259, and TBL2 for TG. We also validated known associations at sub-GWAS significance in FADS2, GATAD2A, PRKCA, and QKI. Exome-based analyses further refined functional variants within these loci and revealed additional known loci in ALDH1A2 for HDL; APOE, APOC1, TM6SF2, CILP2, TOMM40, for LDL and TC; and APOA5, BUD13 for TG and novel loci in ATP8B3, MYH7B, GYS2, and RNF8 for TG. Conditional analysis revealed multiple independent signals at key loci. Gene-based GWAS pinpointed CETP and APOC1 as significant for HDL and LDL, respectively. Rare variant analysis identified significant contribution of loss-of-function missense variants in CETP, TM6SF2, and APOE, in regulating lipid profiles. Associations replicated with consistent directionality in European datasets and Indian adults, reinforcing conserved biology across ancestries and age groups. Functional enrichment analyses emphasized lipid-related pathways and differential expression in liver. These findings lay the foundation for ancestry-informed genetic risk prediction models to identify children at early risk for cardiovascular diseases. - Source: PubMed
Publication date: 2025/08/21
Nair Janaki MBasu AnalabhaTandon NikhilBharadwaj Dwaipayan - Spectroscopic detection of paramagnetically shifted H signals of trivalent lanthanide complexes provide a means for ratiometric detection of enzymatic activity. Herein, we report on the synthesis and characterization of , , and complexes for ratiometric detection of the enzyme nitroreductase (NTR). Ln(III) coordination environments with distinct - and - probe states provide unique paramagnetic contributions to the chemical shift of a 5-(Bu)-pyridine-based reporter group for quantitative detection of enzyme activity. The paramagnetic contribution to chemical shift from Tb(III) and Dy(III) shift the H chemical signal beyond the background region to low frequencies (δ < -15) for zero background signal. Paramagnetic relaxation enhancement of reporter group protons enables the development of probe-specific pulse sequences with short acquisition and delay times. A probe-specific pulse sequence for acquired 256 scans in under 1 min and enabled ratiometric detection of NTR activity. - Source: PubMed
Publication date: 2025/07/11
Kaster Megan ACaldwell Michael ARoach Caroline MBailey Matthew DMeade Thomas J - With their rigid and preorganized skeleton, bispidine (3,7-diazabicyclo[3.3.1]nonane) chelators are very appealing for the preparation of metal complexes with high kinetic inertness. With the aim to develop new Tb(III)-based medical imaging probes, this study describes the synthesis and physicochemical properties of two novel terbium(III) complexes with octadentate bispidine-based ligands substituted with either pyridine-phosphonate (H) or picolinate (H) subunits. Thermodynamic stability constants of the corresponding Tb(III) complexes have been determined by potentiometric, UV-visible absorption spectrophotometric and spectrofluorimetric methods. Despite their apparent similarity, these two octadentate ligands differ in their most stable conformation: - conformation for H and - conformation for H, as confirmed by H NMR studies and suggested by physicochemical investigations. This conformational change induces different protonation schemes for the two ligands. The kinetic inertness of the Tb complexes has been studied in various media and assessed by transmetalation and transchelation experiments. In particular, Tb() displayed a remarkable kinetic inertness with no measurable dissociation over two months in mouse serum at 10 M concentration. The complex was also very inert in the presence of a 50-fold excess of Zn(II) in HO at pH = 7.4 (7% of dissociation over two months). The complexes with ligand are significantly less inert, emphasizing the influence of the ligand conformation on the kinetic inertness of the Ln(III) complexes. Finally, the luminescence properties of the isolated complexes have also been investigated. A bright green luminescence was observed, especially for Tb(), which displays a high quantum yield value of 50% in HO (60% in DO; λ = 263 nm). In addition, luminescence lifetimes of 1.9(2) and 1.7(2) ms have been measured for Tb() and Tb(), respectively, hence confirming the formation of nona-coordinated complexes with one inner-sphere water molecule. These data on a bispidine scaffold pave the way for developing bright, inert luminescent probes for bioimaging and for radiolabeling applications with Tb(III) radioisotopes. - Source: PubMed
Publication date: 2024/11/19
Petitpoisson LucasMahamoud AnliMazan ValérieSy MaryameJeannin OlivierTóth EvaCharbonnière Loïc JElhabiri MouradNonat Aline M - Breast cancer (BC) is a common malignancy that affects women worldwide. Although transducing beta-like 2 (TBL2), a member of the WD40 repeat protein family, has been implicated in various intracellular signaling pathways, its precise function in BC remains unclear. The expression of TBL2 is analyzed using real-time PCR, western blotting, and immunohistochemistry in BC patient specimens. Kaplan-Meier survival analysis is employed to assess its prognostic significance. Proteomic analysis, immunoprecipitation tests, and protein immunoblotting are employed to examine the impact of TBL2 on AKT phosphorylation activation. The findings reveal selective overexpression of TBL2 in BC, correlating significantly with various clinicopathological characteristics and poor survival outcomes in patients with BC. Through in vivo and in vitro experiments, it is observed that TBL2 suppression inhibits BC cell proliferation, while TBL2 overexpression has the opposite effect. Mechanistically, TBL2 is identified as a scaffolding protein that promotes PRMT5 and WDR77 interaction. This interaction enhances the methyltransferase activity of PRMT5, leading to increased AKT phosphorylation activation and promotion of breast cancer cell proliferation. In conclusion, this study uncovers a novel function of TBL2 in the activation of AKT by PRMT5 and suggests TBL2 as a potential therapeutic target for BC treatment. - Source: PubMed
Publication date: 2024/11/05
Lu XiuqingZhang ChaoZhu LeweiWang SifenZeng LijunZhong WenjingWu XuxiaYuan QiTang HailinCui ShienTan YeruLi YuehuaWei Weidong