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TARDBP and amyotrophic lateral sclerosis are reported together in 4 articles.
Gene
TARDBP
- HGNC
- HGNC:11571
4articles
4mentions
0variants with confirmed gene link
Most co-reported phenotypes (articles)
Phenotype
Amyotrophic lateral sclerosis
105articles
105mentions
12co-reported genes shown
Most co-reported genes (articles)
Counts are literature co-mentions in SaudiVarKB, not clinical or causal assertions. Gene details: HGNC; variant status: ClinVar via dbSNP.
Publications
4 records shown · first 60Amyotrophic Lateral Sclerosis (ALS) Genetics and Microbiota: A Comprehensive Review.
PMID 41752118 | PMCID PMC12941290 | DOI 10.3390/ijms27041978 · International journal of molecular sciences · 2026 · 5 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| gene | TARDBP | “Several key genetic factors have been identified, particularly mutations in C9orf72, SOD1, TARDBP, and FUS, which serve as important targets for novel treatments, such as Tofersen, a recently approved SOD1-specific antisense oligonucleotide (ASO) gene therapy.” | 0.98 | hgnc_dict_v1 |
| phenotype | amyotrophic lateral sclerosis | “Amyotrophic Lateral Sclerosis (ALS) Genetics and Microbiota: A Comprehensive Review.” | 0.98 | phenotype_alias_lexicon_v2 |
| gene | C9orf72 | “Several key genetic factors have been identified, particularly mutations in C9orf72, SOD1, TARDBP, and FUS, which serve as important targets for novel treatments, such as Tofersen, a recently approved SOD1-specific antisense oligonucleotide (ASO) gene therapy.” | 0.98 | hgnc_dict_v1 |
| gene | SOD1 | “Several key genetic factors have been identified, particularly mutations in C9orf72, SOD1, TARDBP, and FUS, which serve as important targets for novel treatments, such as Tofersen, a recently approved SOD1-specific antisense oligonucleotide (ASO) gene therapy.” | 0.98 | hgnc_dict_v1 |
CRISPR/Cas9 a genomic engineering technology for treatment in ALS mouse models.
PMID 40837865 | PMCID PMC12362027 | DOI 10.1016/j.reth.2025.07.009 · Regenerative therapy · 2025 · 5 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| gene | TARDBP | “Nearly 20 gene mutations are associated with ALS, with SOD1, FUS, TARDBP, and C9orf72 mutations being more common.” | 0.98 | hgnc_dict_v1 |
| phenotype | amyotrophic lateral sclerosis | “CRISPR/Cas9 a genomic engineering technology for treatment in ALS mouse models.” | 0.93 | phenotype_alias_lexicon_v2 |
| gene | SOD1 | “Nearly 20 gene mutations are associated with ALS, with SOD1, FUS, TARDBP, and C9orf72 mutations being more common.” | 0.98 | hgnc_dict_v1 |
| gene | FUS | “Nearly 20 gene mutations are associated with ALS, with SOD1, FUS, TARDBP, and C9orf72 mutations being more common.” | 0.98 | hgnc_dict_v1 |
Small junction, big problems: Neuromuscular junction pathology in mouse models of amyotrophic lateral sclerosis (ALS).
PMID 34101196 | PMCID PMC9558162 | DOI 10.1111/joa.13463 · Journal of anatomy · 2022 · 4 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| gene | TARDBP | “This review compares the temporal disease progression with severity of disease at the NMJ in mouse models with the most commonly mutated genes in ALS patients (SOD1, C9ORF72, TARDBP and FUS).” | 0.98 | hgnc_dict_v1 |
| phenotype | amyotrophic lateral sclerosis | “Small junction, big problems: Neuromuscular junction pathology in mouse models of amyotrophic lateral sclerosis (ALS).” | 0.98 | phenotype_alias_lexicon_v2 |
| gene | SOD1 | “This review compares the temporal disease progression with severity of disease at the NMJ in mouse models with the most commonly mutated genes in ALS patients (SOD1, C9ORF72, TARDBP and FUS).” | 0.98 | hgnc_dict_v1 |
| gene | FUS | “This review compares the temporal disease progression with severity of disease at the NMJ in mouse models with the most commonly mutated genes in ALS patients (SOD1, C9ORF72, TARDBP and FUS).” | 0.98 | hgnc_dict_v1 |
From Mouse Models to Human Disease: An Approach for Amyotrophic Lateral Sclerosis.
PMID 30150420 | PMCID PMC6199613 | DOI 10.21873/invivo.11339 · In vivo (Athens, Greece) · 2018 · 4 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| gene | TARDBP | “There are several genetic mutations that lead to ALS development, such as chromosome 9 hexanucleotide repeat 72 (C9ORF72), transactive response DNA-binding protein (TARDBP), superoxide dismutase 1 (SOD1) and fused in sarcoma (FUS).” | 0.98 | hgnc_dict_v1 |
| phenotype | amyotrophic lateral sclerosis | “From Mouse Models to Human Disease: An Approach for Amyotrophic Lateral Sclerosis.” | 0.98 | phenotype_alias_lexicon_v2 |
| gene | SOD1 | “There are several genetic mutations that lead to ALS development, such as chromosome 9 hexanucleotide repeat 72 (C9ORF72), transactive response DNA-binding protein (TARDBP), superoxide dismutase 1 (SOD1) and fused in sarcoma (FUS).” | 0.98 | hgnc_dict_v1 |
| gene | FUS | “There are several genetic mutations that lead to ALS development, such as chromosome 9 hexanucleotide repeat 72 (C9ORF72), transactive response DNA-binding protein (TARDBP), superoxide dismutase 1 (SOD1) and fused in sarcoma (FUS).” | 0.98 | hgnc_dict_v1 |