Every reference with a DOI in the deposited reference list resolved to a known
work in Crossref or DataCite at the dated check, and none carried a retraction,
withdrawal, or removal notice.
The 83 checked references that resolve
resolves10.1016/j.celrep.2015.07.059Antagonistic Effects of BACE1 and APH1B-γ-Secretase Control Axonal Guidance by Regulating Growth Cone Collapse
resolves10.1016/j.ajhg.2008.10.008Genome-wide Association Analysis Reveals Putative Alzheimer's Disease Susceptibility Loci in Addition to APOE
resolves10.3233/JAD-2010-1310Follow-Up Study of Susceptibility Loci for Alzheimer's Disease and Onset Age Identified by Genome-Wide Association
resolves10.1242/dev.01103Soluble form of amyloid precursor protein regulates proliferation of progenitors in the adult subventricular zone
resolves10.1038/srep00231The precision of axon targeting of mouse olfactory sensory neurons requires the BACE1 protease
resolves10.1038/ncomms2013Aβ alters the connectivity of olfactory neurons in the absence of amyloid plaques in vivo
resolves10.1016/j.nbd.2012.08.011Constitutive α- and β-secretase cleavages of the amyloid precursor protein are partially coupled in neurons, but not in frequently used cell lines
resolves10.1371/journal.pgen.1001021Partial Loss of Ataxin-1 Function Contributes to Transcriptional Dysregulation in Spinocerebellar Ataxia Type 1 Pathogenesis
resolves10.1002/ana.24792Episodic memory of odors stratifies Alzheimer biomarkers in normal elderly
resolves10.1038/nature09320Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS
resolves10.1038/nm1784Expression of a noncoding RNA is elevated in Alzheimer's disease and drives rapid feed-forward regulation of β-secretase
resolves10.1007/s00415-013-7138-1Longitudinal study of cognitive and psychiatric functions in spinocerebellar ataxia types 1 and 2
resolves10.1016/j.cell.2015.02.012Pumilio1 Haploinsufficiency Leads to SCA1-like Neurodegeneration by Increasing Wild-Type Ataxin1 Levels
resolves10.1126/science.1072994The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics
resolves10.1073/pnas.0710263105Loss of microRNA cluster miR-29a/b-1 in sporadic Alzheimer's disease correlates with increased BACE1/β-secretase expression
resolves10.1074/jbc.m112.415505β-Site Amyloid Precursor Protein (APP)-cleaving Enzyme 1 (BACE1)-deficient Mice Exhibit a Close Homolog of L1 (CHL1) Loss-of-function Phenotype Involving Axon Guidance Defects
resolves10.1038/nn1797Bace1 modulates myelination in the central and peripheral nervous system
resolves10.1093/hmg/ddh019Mutant presenilins specifically elevate the levels of the 42 residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific γ secretase
resolves10.1111/jnc.13632The amyloid cascade hypothesis: are we poised for success or failure?
resolves10.1038/ncb1602BACE1 regulates voltage-gated sodium channels and neuronal activity
resolves10.1038/nn.3614Cell type–specific genetic and optogenetic tools reveal hippocampal CA2 circuits
resolves10.7554/elife.12748Systematic substrate identification indicates a central role for the metalloprotease ADAM10 in axon targeting and synapse function
resolves10.1038/emboj.2012.173Secretome protein enrichment identifies physiological BACE1 protease substrates in neurons
resolves10.1016/j.cell.2006.11.038ATAXIN-1 Interacts with the Repressor Capicua in Its Native Complex to Cause SCA1 Neuropathology
resolves10.1083/jcb.200407070BACE overexpression alters the subcellular processing of APP and inhibits Aβ deposition in vivo
resolves10.1073/pnas.1519156113Neuregulin1 displayed on motor axons regulates terminal Schwann cell-mediated synapse elimination at developing neuromuscular junctions
resolves10.1002/cne.20426Redefining the boundaries of the hippocampal CA2 subfield in the mouse using gene expression and 3‐dimensional reconstruction
resolves10.1038/nature06731Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1
resolves10.1074/jbc.m113.518241MicroRNA-339-5p Down-regulates Protein Expression of β-Site Amyloid Precursor Protein-Cleaving Enzyme 1 (BACE1) in Human Primary Brain Cultures and Is Reduced in Brain Tissue Specimens of Alzheimer Disease Subjects
resolves10.1038/85059Mice deficient in BACE1, the Alzheimer's β-secretase, have normal phenotype and abolished β-amyloid generation
resolves10.1126/science.1248805A Developmental Switch of Axon Targeting in the Continuously Regenerating Mouse Olfactory System
resolves10.1186/s13023-016-0447-6A longitudinal investigation into cognition and disease progression in spinocerebellar ataxia types 1, 2, 3, 6, and 7
resolves10.1074/jbc.m801322200Promotion of BACE1 mRNA Alternative Splicing Reduces Amyloid β-Peptide Production
resolves10.1038/ng0793-221Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1
resolves10.1523/JNEUROSCI.5910-12.2013Postnatal Disruption of the Disintegrin/Metalloproteinase ADAM10 in Brain Causes Epileptic Seizures, Learning Deficits, Altered Spine Morphology, and Defective Synaptic Functions
resolves10.1016/j.jalz.2012.05.213O1‐02‐06: The Alzheimer's beta‐secretase enzyme BACE1 is required for accurate axon guidance of olfactory sensory neurons and normal glomerulus formation in the olfactory bulb
resolves10.1186/1750-1326-10-1Aβ reduction in BACE1 heterozygous null 5XFAD mice is associated with transgenic APP level
resolves10.1038/nature02553Enhanced synaptic plasticity in newly generated granule cells of the adult hippocampus
resolves10.1126/science.286.5440.735β-Secretase Cleavage of Alzheimer's Amyloid Precursor Protein by the Transmembrane Aspartic Protease BACE
resolves10.1371/journal.pone.0105534Intermediate CAG Repeat Expansion in the ATXN2 Gene Is a Unique Genetic Risk Factor for ALS−A Systematic Review and Meta-Analysis of Observational Studies
resolves10.1016/S0896-6273(02)00733-XA Long CAG Repeat in the Mouse Sca1 Locus Replicates SCA1 Features and Reveals the Impact of Protein Solubility on Selective Neurodegeneration
resolves10.1128/MCB.05208-11Impaired Locomotor Learning and Altered Cerebellar Synaptic Plasticity in <i>pep-19/pcp4</i>-Null Mice
resolves10.1074/jbc.m414648200β Subunits of Voltage-gated Sodium Channels Are Novel Substrates of β-Site Amyloid Precursor Protein-cleaving Enzyme (BACE1) and γ-Secretase
resolves10.1093/hmg/10.1.25The spinocerebellar ataxia type 1 protein, ataxin-1, has RNA-binding activity that is inversely affected by the length of its polyglutamine tract
resolves10.1016/j.cell.2013.03.030Integrated Systems Approach Identifies Genetic Nodes and Networks in Late-Onset Alzheimer’s Disease
resolves10.1074/jbc.m109.079079Loss of Function of ATXN1 Increases Amyloid β-Protein Levels by Potentiating β-Secretase Processing of β-Amyloid Precursor Protein
resolves10.1074/jbc.m112.377465The Neural Cell Adhesion Molecules L1 and CHL1 Are Cleaved by BACE1 Protease in Vivo
resolves10.1074/jbc.r800041200Pathogenic Mechanisms of a Polyglutamine-mediated Neurodegenerative Disease, Spinocerebellar Ataxia Type 1
The 13 references without a DOI — listed, not checked
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no DOI — not checkedref7
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no DOI — not checkedref11
no DOI — not checkedFRDA genes in schizophrenic patients and a healthy population
no DOI — not checkedEffect of trinucleotide repeat length and parental sex on phenotypic variation in spinocerebellar ataxia I
no DOI — not checkedGenomic Copy Number Analysis in Alzheimer's Disease and Mild Cognitive Impairment: An ADNI Study
no DOI — not checkedref82
no DOI — not checkedref95
no DOI — not checkedArrow indicates glomeruli, which showed strong immunoreactivity for BACE1. Bottom panel, fluorescence photomicrographs of olfactory glomerulus (arrow) region immunolabeled for Ataxin-1 and BACE1. DAPI was used for nuclear staining. Brain sections from BACE1 KO were used as negative control for the immunofluorescence staining. (C) Analysis of sAPP? (arrow) levels in the cortex and cerebullum of Ataxin-1 WT and KO mouse. Bottom, densitometric quantification of the western blot result (n=3). cerebullum of Ataxin 1 WT and KO mouse
no DOI — not checkedref97
no DOI — not checkedref98
no DOI — not checkedpostnatal (P0, right top) and adult mouse brains. Horizontal straight lines within a blot indicate that different parts within the same blot were placed together. Ataxin-1 levels in the embryonic/postnatal brains were lower than those of adult brains. In contrast, BACE1 levels were much higher in the embryonic/postnatal brains. (bottom panel) No effect of Ataxin-1 depletion on BACE1 levels in cultured cortical neurons (DIV10) and embryonic fibroblasts
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