Ask about this productRelated genes to: BIN1 antibody
- Gene:
- BIN1 NIH gene
- Name:
- bridging integrator 1
- Previous symbol:
- AMPHL
- Synonyms:
- SH3P9, AMPH2
- Chromosome:
- 2q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-19
- Date modifiied:
- 2019-04-23
Related products to: BIN1 antibody
Related articles to: BIN1 antibody
- In laboratory-based diffraction contrast tomography (LabDCT), pixel binning on 2D detectors is an effective strategy to reduce exposure time and improve acquisition efficiency. However, its impact on reconstruction accuracy remains unclear. To address this, we systematically compared LabDCT datasets acquired without detector binning and with 2 × 2 binning, using synchrotron-based DCT (SRDCT) as the ground truth reference. The results show that unbinned (bin1) acquisitions yield higher grain indexing rates and improved grain boundary position accuracy compared with binned data (bin2), particularly for small grains near the sample surface. This improvement is attributed to the longer exposure time, finer spatial sampling (i.e. smaller effective pixel size), and a lower effective detection-size threshold during spot segmentation. To mitigate the information loss induced by binning, we employed a deep-learning spot-segmentation model (Mask R-CNN), which substantially improves reconstructions from binned images and narrows the performance gap relative to unbinned data. Finally, guidelines for further optimization of LabDCT acquisition and reconstruction are proposed. - Source: PubMed
Publication date: 2026/04/19
Ni XinboXia YipingFang HaixingLu JiayiLin FengxiangFan GuohuaZhang Yubin - Alzheimer disease (AD) risk differs across ancestral populations, yet most genetic studies have focused on non-Hispanic White (NHW) cohorts. We conducted a multi-population transcriptome-wide association study (TWAS) using whole-blood RNA sequencing (RNA-seq) and genotype data from NHW (n = 235), African American (AA; n = 224), and Hispanic (HISP; n = 292) Multi-Ancestry Genomics, Epigenomics, and Transcriptomics of Alzheimer's (MAGENTA) participants. Using sum of shared single effects (SuShiE) for multi-population cis-eQTL fine-mapping, we identified credible sets for 8,748 genes, improving fine-mapping precision relative to analyses using fewer populations. cis-eQTL effects were largely shared across populations, with a subset showing population-specific regulation. We performed population-stratified TWAS of AD and inverse-variance-weighted meta-analysis, followed by gene-level TWAS fine-mapping (MA-FOCUS), prioritizing nine genes (false discovery rate [FDR] <0.05, posterior inclusion probability [PIP] >0.8), including established AD loci (BIN1, PTK2B, DMPK) with broadly consistent effects across populations. At BIN1, fine-mapped cis-eQTL variants used in the TWAS prediction model highlighted rs11682128, which is only modestly correlated with the genome-wide association study (GWAS) index SNP rs6733839 (r ≈ 0.34), demonstrating how integrating eQTL fine-mapping with TWAS can refine signals beyond sentinel GWAS variants. We also identified an association between COG4 expression and AD in NHW, implicating Golgi-related pathways. Using independent SuShiE-derived models from TOPMed MESA (PBMC), several signals replicated directionally across ancestries, with the strongest statistical support in NHW. Overall, multi-population eQTL fine-mapping improves model interpretability and helps resolve shared and population-specific regulatory mechanisms relevant to AD. - Source: PubMed
Publication date: 2026/04/30
Sun XinyuMews MakaelaWheeler Nicholas RBenchek PenelopeGu TianjieGomez LissetteRay NicholasReitz ChristianeNaj Adam CBelow Jennifer ElizabethTosto GiuseppeCornejo-Olivas MarioByrd Goldie SFeliciano-Astacio Briseida ECelis KatrinaRajabli FaridKunkle Brian WPericak-Vance Margaret AHaines Jonathan LGriswold Anthony JBush William S - The MYC family of transforming oncogenes function as regulators of gene transcription and is composed of three members, MYC, MYCN and MYCL. As c-MYC (MYC) is deregulated in >50% of human cancers, the role, regulation and structural features of MYC have been well-studied. By contrast, L-MYC has been understudied as historically, oncogenic deregulation was evident only in a subset of lung carcinomas. However, recent deep genomic analyses of primary patient samples has demonstrated that L-MYC is deregulated in numerous human cancers. With this revelation it is important to understand how L-MYC compares to MYC at the structural level, particularly for the development of broad-spectrum inhibitors of the MYC family. Here we show that L-MYC expression is elevated in several primary patient tumor samples, providing further evidence for L-MYC as a driver oncoprotein in primary human cancers. Next, we provide new biophysical insights into an N-terminal region within the L-MYC transactivation domain, which harbors two regions conserved amongst MYC proteins: MYC box 0 (MB0) and MYC box I (MBI). NMR spectroscopy of residues 1-80 of L-MYC confirms that it is largely intrinsically disordered and interacts with the known MYC-MB0 interactor, PNUTS (Phosphatase 1 NUclear Targeting Subunit). Comparatively, L-MYC does not interact with the MYC-MBI interactor and tumor suppressor Bin1 (Bridging integrator 1). Together, these results further substantiate the oncogenic role of L-MYC in human cancer and enhance our understanding of the biophysical nature of L-MYC to improve strategies for the development of anti-cancer therapeutics targeting MYC family members. - Source: PubMed
Publication date: 2026/04/24
Kenney Tristan MgHouliston ScottLin PeterMovahedi NikanArrowsmith CherylPenn Linda Z - Most existing transcriptome wide association studies (TWASs) of Alzheimer's Disease (AD) dementia only use bulk RNA-seq data and a single statistical method. Here, we utilize an omnibus TWAS (TWAS-O) pipeline that leverages multiple complementary statistical methods to integrate the snRNA-seq dataset (n = 415) of the dorsolateral prefrontal cortex (DLPFC) and the latest GWAS data of AD dementia. We fine-map TWAS risk genes by gene-based conditional analysis and conducted validation analyses by the analogous omnibus proteome-wide association studies (PWAS-O) using bulk proteomics data of DLPFC (n = 716). We identify 223 unique cell-type-aware TWAS risk genes from 350 associations across six major brain cell-types, including 91 fine-mapped independent associations, 11 of which are novel. By PWAS-O, we identify 21 significant PWAS risk genes, including 13 independent associations, which validated 31.9% independent cell-type-aware TWAS associations. By protein-protein interaction network analyses, our novel cell-type-aware TWAS findings are linked to established AD risk genes such as APOE, BIN1, and MAPT. - Source: PubMed
Publication date: 2026/04/22
Liu QiangParrish Randy LTang ShizhenTasaki ShinyaBennett David ASeyfried Nicholas TDe Jager Philip LMenon VilasBuchman Aron SYang Jingjing - Cerebrospinal fluid amyloid beta 42, total tau, and phosphorylated tau 181 are well accepted markers of Alzheimer's disease. These biomarkers better reflect disease pathogenesis compared to clinical diagnosis. Here, we perform a genome wide association study meta-analysis including 18,948 individuals of European ancestry and identify 12 genome-wide significant loci across all three biomarkers, eight of them novel. We replicate the association of biomarkers with APOE, CR1, GMNC/CCDC50 and C16orf95/MAP1LC3B. Novel loci include BIN1 for amyloid beta and GNA12, MS4A6A, SLCO1A2 with both total tau and phosphorylated tau 181, as well as additional loci on chr. 8, near ANGPT1 and chr. 9 near SMARCA2. We also demonstrate that these variants have significant association with Alzheimer's disease risk, disease progression and/or brain amyloidosis. The associated genes are implicated in lipid metabolism independent of APOE, coupled with autophagy and brain volume regulation driven by total tau and phosphorylated tau 181 dysregulation. - Source: PubMed
Publication date: 2026/04/21
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