On the public citation graph

TDP43 autoregulation gives rise to shortened isoforms that are tightly controlled by both transcriptional and post-translational mechanisms

https://doi.org/10.1101/2024.07.02.601776

0 signed · 113 inferred · view as graph

Inferred edges come from two machine sources: sweeps of open repository metadata (mostly SSRN and Zenodo), and a bulk OpenAlex citation snapshot. Every row below is labelled with the one it came from. Neither is a complete citation index — absence here is not evidence of absence.

Is this your work? Sign in with ORCID and put your name on the claims that are yours.

Claim with ORCID

Reference health. See whether every reference in this work resolves to a known work and none has been retracted — and get a dated CiteStamped badge you can embed.

See reference health

What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

inferredcites →https://doi.org/10.1001/jamaneurol.2015.1872openalex-snapshot

Cortical Function in Asymptomatic Carriers and Patients WithC9orf72Amyotrophic Lateral Sclerosis

inferredcites →https://doi.org/10.1002/(sici)1097-4598(199701)20:1<65::aid-mus9>3.0.co;2-fopenalex-snapshot

Abnormalities of cortical inhibitory neurons in amyotrophic lateral sclerosis

inferredcites →https://doi.org/10.1002/acn3.51039openalex-snapshot

Cortical hyperexcitability evolves with disease progression in ALS

inferredcites →https://doi.org/10.1002/alz.13915openalex-snapshot

An ANXA11 P93S variant dysregulates TDP‐43 and causes corticobasal syndrome

inferredcites →https://doi.org/10.1002/cpcb.51openalex-snapshot

Transcription Factor–Mediated Differentiation of Human iPSCs into Neurons

inferredcites →https://doi.org/10.1002/cpz1.344openalex-snapshot

Measuring mRNA Decay with Roadblock‐qPCR

inferredcites →https://doi.org/10.1007/s00401-010-0659-0openalex-snapshot

Loss of murine TDP-43 disrupts motor function and plays an essential role in embryogenesis

inferredcites →https://doi.org/10.1007/s00401-023-02599-5openalex-snapshot

Cryptic exon detection and transcriptomic changes revealed in single-nuclei RNA sequencing of C9ORF72 patients spanning the ALS-FTD spectrum

inferredcites →https://doi.org/10.1007/s00401-023-02655-0openalex-snapshot

Cryptic splicing of stathmin-2 and UNC13A mRNAs is a pathological hallmark of TDP-43-associated Alzheimer’s disease

inferredcites →https://doi.org/10.1007/s12031-011-9625-0openalex-snapshot

Progranulin and TDP-43: Mechanistic Links and Future Directions

inferredcites →https://doi.org/10.1016/j.bbrc.2006.10.093openalex-snapshot

TDP-43 is a component of ubiquitin-positive tau-negative inclusions in frontotemporal lobar degeneration and amyotrophic lateral sclerosis

inferredcites →https://doi.org/10.1016/j.bbrc.2012.07.071openalex-snapshot

The N-terminus of TDP-43 promotes its oligomerization and enhances DNA binding affinity

inferredcites →https://doi.org/10.1016/j.bmcl.2012.08.107openalex-snapshot

Identification of pyrimidine derivatives as hSMG-1 inhibitors

inferredcites →https://doi.org/10.1016/j.celrep.2019.03.093openalex-snapshot

An Intramolecular Salt Bridge Linking TDP43 RNA Binding, Protein Stability, and TDP43-Dependent Neurodegeneration

inferredcites →https://doi.org/10.1016/j.celrep.2019.04.003openalex-snapshot

Loss of Nuclear TDP-43 Is Associated with Decondensation of LINE Retrotransposons

inferredcites →https://doi.org/10.1016/j.celrep.2021.108925openalex-snapshot

UPF1 reduces C9orf72 HRE-induced neurotoxicity in the absence of nonsense-mediated decay dysfunction

inferredcites →https://doi.org/10.1016/j.celrep.2021.109376openalex-snapshot

Human oncoprotein 5MP suppresses general and repeat-associated non-AUG translation via eIF3 by a common mechanism

inferredcites →https://doi.org/10.1016/j.cub.2022.04.053openalex-snapshot

Myotubularin-related phosphatase 5 is a critical determinant of autophagy in neurons

inferredcites →https://doi.org/10.1016/j.expneurol.2009.08.017openalex-snapshot

Defining the mechanisms that underlie cortical hyperexcitability in amyotrophic lateral sclerosis

inferredcites →https://doi.org/10.1016/j.febslet.2006.01.052openalex-snapshot

TDP43 depletion rescues aberrant CFTR exon 9 skipping

inferredcites →https://doi.org/10.1016/j.jbc.2021.101003openalex-snapshot

Development of a specific live-cell assay for native autophagic flux

inferredcites →https://doi.org/10.1016/j.molcel.2022.12.019openalex-snapshot

RNA methylation influences TDP43 binding and disease pathogenesis in models of amyotrophic lateral sclerosis and frontotemporal dementia

inferredcites →https://doi.org/10.1016/j.neuron.2011.09.010openalex-snapshot

A Hexanucleotide Repeat Expansion in C9ORF72 Is the Cause of Chromosome 9p21-Linked ALS-FTD

inferredcites →https://doi.org/10.1016/j.neuron.2011.09.011openalex-snapshot

Expanded GGGGCC Hexanucleotide Repeat in Noncoding Region of C9ORF72 Causes Chromosome 9p-Linked FTD and ALS

inferredcites →https://doi.org/10.1016/j.neuron.2019.07.014openalex-snapshot

CRISPR Interference-Based Platform for Multimodal Genetic Screens in Human iPSC-Derived Neurons

inferredcites →https://doi.org/10.1016/j.omtm.2016.12.007openalex-snapshot

Simple Derivation of Spinal Motor Neurons from ESCs/iPSCs Using Sendai Virus Vectors

inferredcites →https://doi.org/10.1016/j.tcb.2016.05.004openalex-snapshot

Principles and Properties of Stress Granules

inferredcites →https://doi.org/10.1016/s0888-7543(03)00214-3openalex-snapshot

Structural diversity and functional implications of the eukaryotic TDP gene family

inferredcites →https://doi.org/10.1016/s1388-2457(02)00288-2openalex-snapshot

Different mechanisms contribute to motor cortex hyperexcitability in amyotrophic lateral sclerosis

inferredcites →https://doi.org/10.1021/acs.biochem.7b01162openalex-snapshot

P-Bodies: Composition, Properties, and Functions

inferredcites →https://doi.org/10.1038/emboj.2010.310openalex-snapshot

TDP‐43 regulates its mRNA levels through a negative feedback loop

inferredcites →https://doi.org/10.1038/gt.2014.101openalex-snapshot

Preservation of forelimb function by UPF1 gene therapy in a rat model of TDP-43-induced motor paralysis

inferredcites →https://doi.org/10.1038/mt.2009.3openalex-snapshot

Mimicking Aspects of Frontotemporal Lobar Degeneration and Lou Gehrig's Disease in Rats via TDP-43 Overexpression

inferredcites →https://doi.org/10.1038/mt.2013.88openalex-snapshot

Selective Forelimb Impairment in Rats Expressing a Pathological TDP-43 25 kDa C-terminal Fragment to Mimic Amyotrophic Lateral Sclerosis

inferredcites →https://doi.org/10.1038/nature02998openalex-snapshot

Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death

inferredcites →https://doi.org/10.1038/nature10353openalex-snapshot

Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia

inferredcites →https://doi.org/10.1038/nature11922openalex-snapshot

Mutations in prion-like domains in hnRNPA2B1 and hnRNPA1 cause multisystem proteinopathy and ALS

inferredcites →https://doi.org/10.1038/nbt1191openalex-snapshot

Engineering of a monomeric green-to-red photoactivatable fluorescent protein induced by blue light

inferredcites →https://doi.org/10.1038/nchembio.1308openalex-snapshot

Proteostasis of polyglutamine varies among neurons and predicts neurodegeneration

inferredcites →https://doi.org/10.1038/nchembio.1563openalex-snapshot

Autophagy induction enhances TDP43 turnover and survival in neuronal ALS models

inferredcites →https://doi.org/10.1038/nchembio.304openalex-snapshot

Inhibition of eukaryotic translation elongation by cycloheximide and lactimidomycin

inferredcites →https://doi.org/10.1038/nn.2778openalex-snapshot

Characterizing the RNA targets and position-dependent splicing regulation by TDP-43

inferredcites →https://doi.org/10.1038/nn.2779openalex-snapshot

Long pre-mRNA depletion and RNA missplicing contribute to neuronal vulnerability from loss of TDP-43

inferredcites →https://doi.org/10.1038/nn.4000openalex-snapshot

Haploinsufficiency of TBK1 causes familial ALS and fronto-temporal dementia

inferredcites →https://doi.org/10.1038/nprot.2013.143openalex-snapshot

Genome engineering using the CRISPR-Cas9 system

inferredcites →https://doi.org/10.1038/s41467-017-00062-0openalex-snapshot

Functional and dynamic polymerization of the ALS-linked protein TDP-43 antagonizes its pathologic aggregation

inferredcites →https://doi.org/10.1038/s41586-022-04424-7openalex-snapshot

TDP-43 represses cryptic exon inclusion in the FTD–ALS gene UNC13A

inferredcites →https://doi.org/10.1038/s41586-022-04436-3openalex-snapshot

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

inferredcites →https://doi.org/10.1038/s41593-018-0113-5openalex-snapshot

TDP-43 gains function due to perturbed autoregulation in a Tardbp knock-in mouse model of ALS-FTD

inferredcites →https://doi.org/10.1038/s41593-018-0293-zopenalex-snapshot

Premature polyadenylation-mediated loss of stathmin-2 is a hallmark of TDP-43-dependent neurodegeneration

inferredcites →https://doi.org/10.1038/s41593-018-0300-4openalex-snapshot

ALS-implicated protein TDP-43 sustains levels of STMN2, a mediator of motor neuron growth and repair

inferredcites →https://doi.org/10.1038/s41598-018-22858-wopenalex-snapshot

TDP43 nuclear export and neurodegeneration in models of amyotrophic lateral sclerosis and frontotemporal dementia

inferredcites →https://doi.org/10.1073/pnas.0912417107openalex-snapshot

TDP-43 transgenic mice develop spastic paralysis and neuronal inclusions characteristic of ALS and frontotemporal lobar degeneration

inferredcites →https://doi.org/10.1073/pnas.0913602107openalex-snapshot

A Drosophila model for TDP-43 proteinopathy

inferredcites →https://doi.org/10.1073/pnas.1008227107openalex-snapshot

ALS-associated mutations in TDP-43 increase its stability and promote TDP-43 complexes with FUS/TLS

inferredcites →https://doi.org/10.1073/pnas.1218311110openalex-snapshot

Loss of ALS-associated TDP-43 in zebrafish causes muscle degeneration, vascular dysfunction, and reduced motor neuron axon outgrowth

inferredcites →https://doi.org/10.1073/pnas.1509744112openalex-snapshot

Amelioration of toxicity in neuronal models of amyotrophic lateral sclerosis by hUPF1

inferredcites →https://doi.org/10.1073/pnas.221303298openalex-snapshot

A conditional tissue-specific transgene expression system using inducible GAL4

inferredcites →https://doi.org/10.1074/jbc.m104236200openalex-snapshot

Characterization and Functional Implications of the RNA Binding Properties of Nuclear Factor TDP-43, a Novel Splicing Regulator ofCFTR Exon 9

inferredcites →https://doi.org/10.1074/jbc.m109.061846openalex-snapshot

TDP-43 Is a Developmentally Regulated Protein Essential for Early Embryonic Development

inferredcites →https://doi.org/10.1074/jbc.m112.359000openalex-snapshot

Targeted Depletion of TDP-43 Expression in the Spinal Cord Motor Neurons Leads to the Development of Amyotrophic Lateral Sclerosis-like Phenotypes in Mice

inferredcites →https://doi.org/10.1074/mcp.m800390-mcp200openalex-snapshot

Multiplex SILAC Analysis of a Cellular TDP-43 Proteinopathy Model Reveals Protein Inclusions Associated with SUMOylation and Diverse Polyubiquitin Chains

inferredcites →https://doi.org/10.1083/jcb.147.7.1431openalex-snapshot

RNA-Binding Proteins Tia-1 and Tiar Link the Phosphorylation of Eif-2α to the Assembly of Mammalian Stress Granules

inferredcites →https://doi.org/10.1093/brain/awl024openalex-snapshot

Altered axonal excitability properties in amyotrophic lateral sclerosis: impaired potassium channel function related to disease stage

inferredcites →https://doi.org/10.1093/brain/awn071openalex-snapshot

Cortical hyperexcitability may precede the onset of familial amyotrophic lateral sclerosis

inferredcites →https://doi.org/10.1093/brain/awr159openalex-snapshot

Pathological hallmarks of amyotrophic lateral sclerosis/frontotemporal lobar degeneration in transgenic mice produced with TDP-43 genomic fragments

inferredcites →https://doi.org/10.1093/brain/awr348openalex-snapshot

Non-human primate model of amyotrophic lateral sclerosis with cytoplasmic mislocalization of TDP-43

inferredcites →https://doi.org/10.1093/brain/awt029openalex-snapshot

Loss of TDP-43 causes age-dependent progressive motor neuron degeneration

inferredcites →https://doi.org/10.1093/cercor/bhw177openalex-snapshot

Cholinergic Surveillance over Hippocampal RNA Metabolism and Alzheimer's-Like Pathology

inferredcites →https://doi.org/10.1093/emboj/20.7.1785openalex-snapshot

SC35 autoregulates its expression by promoting splicing events that destabilize its mRNAs

inferredcites →https://doi.org/10.1093/hmg/ddp534openalex-snapshot

Gain and loss of function of ALS-related mutations of TARDBP (TDP-43) cause motor deficits in vivo

inferredcites →https://doi.org/10.1093/hmg/ddr124openalex-snapshot

Wild-type and A315T mutant TDP-43 exert differential neurotoxicity in a Drosophila model of ALS

inferredcites →https://doi.org/10.1093/hmg/ddt005openalex-snapshot

Loss and gain of Drosophila TDP-43 impair synaptic efficacy and motor control leading to age-related neurodegeneration by loss-of-function phenotypes

inferredcites →https://doi.org/10.1093/jmcb/mjab022openalex-snapshot

Regulation of nonsense-mediated mRNA decay in neural development and disease

inferredcites →https://doi.org/10.1093/nar/gkae655openalex-snapshot

Stress granule formation helps to mitigate neurodegeneration

inferredcites →https://doi.org/10.1093/nar/gkw499openalex-snapshot

Increased cytoplasmicTARDBPmRNA in affected spinal motor neurons in ALS caused by abnormal autoregulation of TDP-43

inferredcites →https://doi.org/10.1097/nen.0b013e31803020b9openalex-snapshot

TDP-43 in the Ubiquitin Pathology of Frontotemporal Dementia With VCP Gene Mutations

inferredcites →https://doi.org/10.1097/pat.0b013e3283426eeeopenalex-snapshot

Overview and recent advances in neuropathology. Part 2: Neurodegeneration

inferredcites →https://doi.org/10.1101/gad.194829.112openalex-snapshot

Autoregulation of TDP-43 mRNA levels involves interplay between transcription, splicing, and alternative polyA site selection

inferredcites →https://doi.org/10.1104/pp.55.5.815openalex-snapshot

Cycloheximide Is Not a Specific Inhibitor of Protein Synthesis in Vivo

inferredcites →https://doi.org/10.1111/ene.16281openalex-snapshot

Reduction in short interval intracortical inhibition from the early stage reflects the pathophysiology in amyotrophic lateral sclerosis: A meta‐analysis study

inferredcites →https://doi.org/10.1111/jmp.12162openalex-snapshot

Initial gene vector dosing for studying symptomatology of amyotrophic lateral sclerosis in non‐human primates

inferredcites →https://doi.org/10.1111/neup.12233openalex-snapshot

Clinicopathological description of two cases with SQSTM1 gene mutation associated with frontotemporal dementia

inferredcites →https://doi.org/10.1126/science.1134108openalex-snapshot

Ubiquitinated TDP-43 in Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis

inferredcites →https://doi.org/10.1126/science.aab0983openalex-snapshot

TDP-43 repression of nonconserved cryptic exons is compromised in ALS-FTD

inferredcites →https://doi.org/10.1126/scitranslmed.adg7162openalex-snapshot

Mis-spliced transcripts generate de novo proteins in TDP-43–related ALS/FTD

inferredcites →https://doi.org/10.1136/jnnp-2011-301782openalex-snapshot

Motor axonal excitability properties are strong predictors for survival in amyotrophic lateral sclerosis

inferredcites →https://doi.org/10.1172/jci130988openalex-snapshot

Shortened TDP43 isoforms upregulated by neuronal hyperactivity drive TDP43 pathology in ALS

inferredcites →https://doi.org/10.1172/jci139741openalex-snapshot

Truncated stathmin-2 is a marker of TDP-43 pathology in frontotemporal dementia

inferredcites →https://doi.org/10.1186/s12920-017-0274-1openalex-snapshot

Quantitative analysis of cryptic splicing associated with TDP-43 depletion

inferredcites →https://doi.org/10.1242/dev.165753openalex-snapshot

Third-generation in situ hybridization chain reaction: multiplexed, quantitative, sensitive, versatile, robust

inferredcites →https://doi.org/10.1261/rna.047647.114openalex-snapshot

Studies of alternative isoforms provide insight into TDP-43 autoregulation and pathogenesis

inferredcites →https://doi.org/10.1261/rna.059055.116openalex-snapshot

Transcriptome-wide identification of NMD-targeted human mRNAs reveals extensive redundancy between SMG6- and SMG7-mediated degradation pathways

inferredcites →https://doi.org/10.1261/rna.7258505openalex-snapshot

Processing bodies require RNA for assembly and contain nontranslating mRNAs

inferredcites →https://doi.org/10.1371/journal.pbio.1001052openalex-snapshot

A Yeast Model of FUS/TLS-Dependent Cytotoxicity

inferredcites →https://doi.org/10.1371/journal.pone.0012247openalex-snapshot

TDP-43-Mediated Neuron Loss In Vivo Requires RNA-Binding Activity

inferredcites →https://doi.org/10.1371/journal.pone.0038658openalex-snapshot

Coaggregation of RNA-Binding Proteins in a Model of TDP-43 Proteinopathy with Selective RGG Motif Methylation and a Role for RRM1 Ubiquitination

inferredcites →https://doi.org/10.1371/journal.pone.0169506openalex-snapshot

Functional Maturation of Human Stem Cell-Derived Neurons in Long-Term Cultures

inferredcites →https://doi.org/10.1523/eneuro.0249-16.2017openalex-snapshot

The Proline/Arginine Dipeptide from Hexanucleotide Repeat ExpandedC9ORF72Inhibits the Proteasome

inferredcites →https://doi.org/10.1523/jneurosci.0146-10.2010openalex-snapshot

Quantitative Relationships between Huntingtin Levels, Polyglutamine Length, Inclusion Body Formation, and Neuronal Death Provide Novel Insight into Huntington's Disease Molecular Pathogenesis

inferredcites →https://doi.org/10.1523/jneurosci.4988-09.2010openalex-snapshot

Cytoplasmic Mislocalization of TDP-43 Is Toxic to Neurons and Enhanced by a Mutation Associated with Familial Amyotrophic Lateral Sclerosis

inferredcites →https://doi.org/10.15252/embj.201797452openalex-snapshot

A single N‐terminal phosphomimic disrupts TDP‐43 polymerization, phase separation, and RNA splicing

inferredcites →https://doi.org/10.15252/embr.201847498openalex-snapshot

DDX3X and specific initiation factors modulate FMR1 repeat‐associated non‐AUG‐initiated translation

inferredcites →https://doi.org/10.15252/msb.20145508openalex-snapshot

Rapid neurogenesis through transcriptional activation in human stem cells

inferredcites →https://doi.org/10.1534/genetics.119.302985openalex-snapshot

Amyotrophic Lateral Sclerosis Modifiers inDrosophilaReveal the Phospholipase D Pathway as a Potential Therapeutic Target

inferredcites →https://doi.org/10.21105/joss.01317openalex-snapshot

lifelines: survival analysis in Python

inferredcites →https://doi.org/10.3389/fendo.2018.00790openalex-snapshot

Hallmarks of Aging: An Autophagic Perspective

inferredcites →https://doi.org/10.3389/fnins.2022.818655openalex-snapshot

TDP-43 Oligomerization and Phase Separation Properties Are Necessary for Autoregulation

inferredcites →https://doi.org/10.3389/fnins.2022.868556openalex-snapshot

A C-Terminally Truncated TDP-43 Splice Isoform Exhibits Neuronal Specific Cytoplasmic Aggregation and Contributes to TDP-43 Pathology in ALS

inferredcites →https://doi.org/10.3791/59036openalex-snapshot

Monitoring Neuronal Survival via Longitudinal Fluorescence Microscopy

inferredcites →https://doi.org/10.5281/zenodo.3497105openalex-snapshot

Computer Vision Annotation Tool

inferredcites →https://doi.org/10.7554/elife.35977openalex-snapshot

Matrin 3-dependent neurotoxicity is modified by nucleic acid binding and nucleocytoplasmic localization

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

inferred← citeshttps://doi.org/10.1101/2025.04.07.646890openalex-snapshot

Context-dependent Interactors Regulate TDP-43 Dysfunction in ALS/FTLD

Editorial review for independent work. ICSAC — the Institute for Complexity Science and Advanced Computing — runs a structured editorial panel for researchers publishing outside journals, and publishes on CiteStamp rails. Submission is free and goes through ORCID: icsacinstitute.org/submit.