KDM6A-Mediated H3K27me3 Rejuvenation
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From Analysis:
Epigenetic clocks and biological aging in neurodegeneration
Epigenetic clocks and biological aging in neurodegeneration
Hypotheses from Same Analysis (5)
These hypotheses emerged from the same multi-agent debate that produced this hypothesis.
Description
Molecular Mechanism and Rationale
The lysine demethylase 6A (KDM6A), also known as UTX (Ubiquitously Transcribed Tetratricopeptide Repeat, X chromosome), represents a critical epigenetic regulator that catalyzes the removal of repressive histone H3 lysine 27 trimethylation (H3K27me3) marks through its Jumonji C (JmjC) domain-containing demethylase activity. This chromatin-modifying enzyme functions as part of the larger COMPASS-like complexes and operates in direct opposition to the Polycomb Repressive Complex 2 (PRC2), which deposits H3K27me3 marks via its catalytic subunit EZH2 (Enhancer of Zeste Homolog 2).
...Figures & Visualizations
Curated Mechanism Pathway
Curated pathway diagram from expert analysis
graph TD
A["KDM6A<br/>(UTX)"]
B["H3K27me3<br/>Repressive Marks"]
C["Alpha-ketoglutarate<br/>Co-substrate"]
D["Ascorbic Acid<br/>(Vitamin C)"]
E["PRC2/EZH2<br/>Complex"]
F["Chromatin<br/>Remodeling"]
G["Gene<br/>Transcription"]
H["Neuronal Survival<br/>Genes"]
I["Synaptic Plasticity<br/>Genes"]
J["COMPASS-like<br/>Complexes"]
K["Transcriptional<br/>Repression"]
L["Neurodegeneration<br/>Pathology"]
M["Cognitive<br/>Function"]
N["Therapeutic<br/>Intervention"]
O["Succinate and CO2<br/>Byproducts"]
N -->|"Enhances"| A
A -->|"Requires"| C
A -->|"Requires"| D
A -->|"Demethylates"| B
A -->|"Associates with"| J
A -->|"Produces"| O
E -->|"Deposits"| B
B -->|"Causes"| K
A -->|"Removes marks"| F
F -->|"Activates"| G
G -->|"Upregulates"| H
G -->|"Upregulates"| I
K -->|"Silences"| H
K -->|"Silences"| I
K -->|"Leads to"| L
H -->|"Maintains"| M
I -->|"Supports"| M
L -->|"Impairs"| M
classDef normal fill:#4fc3f7
classDef therapeutic fill:#81c784
classDef pathology fill:#ef5350
classDef outcome fill:#ffd54f
classDef molecular fill:#ce93d8
class A,C,D,J,F,G,O molecular
class N therapeutic
class B,E,K,L pathology
class M outcome
class H,I normal
3D Protein Structure
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Dimension Scores
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✓ Supporting Evidence 14
Topoisomerases are crucial for solving DNA topological problems, but they have not been linked to RNA metabolism. Here we show that human topoisomerase 3β (Top3β) is an RNA topoisomerase that biochemically and genetically interacts with FMRP, a protein that is deficient in fragile X syndrome and is known to regulate the translation of mRNAs that are important for neuronal function, abnormalities of which are linked to autism. Notably, the FMRP-Top3β interaction is abolished by a disease-associated mutation of FMRP, suggesting that Top3β may contribute to the pathogenesis of mental disorders. Top3β binds multiple mRNAs encoded by genes with neuronal functions linked to schizophrenia and autism. Expression of one such gene, that encoding protein tyrosine kinase 2 (ptk2, also known as focal adhesion kinase or FAK), is reduced in the neuromuscular junctions of Top3β mutant flies. Synapse formation is defective in Top3β mutant flies and mice, as well as in FMRP mutant flies and mice. Our fi
Lysine acetylation is a widespread post-translational modification regulating various biological processes. To characterize cellular functions of the human lysine acetyltransferases KAT2A (GCN5) and KAT2B (PCAF), we determined their acetylome by shotgun proteomics. One of the newly identified KAT2A/2B substrate is polo-like kinase 4 (PLK4), a key regulator of centrosome duplication. We demonstrate that KAT2A/2B acetylate the PLK4 kinase domain on residues K45 and K46. Molecular dynamics modelling suggests that K45/K46 acetylation impairs kinase activity by shifting the kinase to an inactive conformation. Accordingly, PLK4 activity is reduced upon in vitro acetylation of its kinase domain. Moreover, the overexpression of the PLK4 K45R/K46R mutant in cells does not lead to centrosome overamplification, as observed with wild-type PLK4. We also find that impairing KAT2A/2B-acetyltransferase activity results in diminished phosphorylation of PLK4 and in excess centrosome numbers in cells. Ov
Megalencephaly-capillary malformation (MCAP) and megalencephaly-polymicrogyria-polydactyly-hydrocephalus (MPPH) syndromes are sporadic overgrowth disorders associated with markedly enlarged brain size and other recognizable features. We performed exome sequencing in 3 families with MCAP or MPPH, and our initial observations were confirmed in exomes from 7 individuals with MCAP and 174 control individuals, as well as in 40 additional subjects with megalencephaly, using a combination of Sanger sequencing, restriction enzyme assays and targeted deep sequencing. We identified de novo germline or postzygotic mutations in three core components of the phosphatidylinositol 3-kinase (PI3K)-AKT pathway. These include 2 mutations in AKT3, 1 recurrent mutation in PIK3R2 in 11 unrelated families with MPPH and 15 mostly postzygotic mutations in PIK3CA in 23 individuals with MCAP and 1 with MPPH. Our data highlight the central role of PI3K-AKT signaling in vascular, limb and brain development and emp
Highly active antiretroviral therapy (HAART) is the only available remedial measure to treat HIV infected patients, as recognized by the WHO. However, it is associated with toxicity (nephrotoxicity), high cost and most preferably drug resistance in the first-line treatment. Wherefore, potential and novel natural source is the only option for the modern world to challenge this global issue. In recent years, sulfated polysaccharide from marine macroalgae shown to be biologically active as anti-inflammatory, anticoagulant, antitumor, immunomodulatory and antiviral agents. As a direct inhibitor of HIV including other retroviruses, it is considered as a "new generation antiretroviral drug". In our present study, Fucoidan, a sulfated polysaccharide has been extracted from two different macroalgae Dictyota bartayesiana (DD) and Turbinaria decurrens (TD) based on hot water extraction method and further confirmed by FT-IR and RP-HPLC methods. Both the crude and purified fucoidan samples were ev
Generation of the "epitranscriptome" through post-transcriptional ribonucleoside modification embeds a layer of regulatory complexity into RNA structure and function. Here, we describe N4-acetylcytidine (ac4C) as an mRNA modification that is catalyzed by the acetyltransferase NAT10. Transcriptome-wide mapping of ac4C revealed discretely acetylated regions that were enriched within coding sequences. Ablation of NAT10 reduced ac4C detection at the mapped mRNA sites and was globally associated with target mRNA downregulation. Analysis of mRNA half-lives revealed a NAT10-dependent increase in stability in the cohort of acetylated mRNAs. mRNA acetylation was further demonstrated to enhance substrate translation in vitro and in vivo. Codon content analysis within ac4C peaks uncovered a biased representation of cytidine within wobble sites that was empirically determined to influence mRNA decoding efficiency. These findings expand the repertoire of mRNA modifications to include an acetylated
Integral membrane proteins are encoded by approximately 25% of all protein-coding genes1. In eukaryotes, the majority of membrane proteins are inserted, modified and folded at the endoplasmic reticulum (ER)2. Research over the past several decades has determined how membrane proteins are targeted to the ER and how individual transmembrane domains (TMDs) are inserted into the lipid bilayer3. By contrast, very little is known about how multi-spanning membrane proteins with several TMDs are assembled within the membrane. During the assembly of TMDs, interactions between polar or charged amino acids typically stabilize the final folded configuration4-8. TMDs with hydrophilic amino acids are likely to be chaperoned during the co-translational biogenesis of membrane proteins; however, ER-resident intramembrane chaperones are poorly defined. Here we identify the PAT complex, an abundant obligate heterodimer of the widely conserved ER-resident membrane proteins CCDC47 and Asterix. The PAT comp
The hallmark of gram-negative bacteria and organelles such as mitochondria and chloroplasts is the presence of an outer membrane. In bacteria such as Escherichia coli, the outer membrane is a unique asymmetric lipid bilayer with lipopolysaccharide in the outer leaflet. Integral transmembrane proteins assume a β-barrel structure, and their assembly is catalyzed by the heteropentameric Bam complex containing the outer membrane protein BamA and four lipoproteins, BamB-E. How the Bam complex assembles a great diversity of outer membrane proteins into a membrane without an obvious energy source is a particularly challenging problem, because folding intermediates are predicted to be unstable in either an aqueous or a hydrophobic environment. Two models have been put forward: the budding model, based largely on structural data, and the BamA assisted model, based on genetic and biochemical studies. Here we offer a critical discussion of the pros and cons of each.
Infection or vaccination induces a population of long-lived bone marrow plasma cells (BMPCs) that are a persistent and essential source of protective antibodies1-5. Whether this population is induced in patients infected with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is unknown. Recent reports have suggested that SARS-CoV-2 convalescent patients experience a rapid decay in their antigen-specific serum antibodies, raising concerns that humoral immunity against this virus may be short-lived6-8. Here we show that in patients who experienced mild infections (n=73), serum anti-SARS-CoV-2 spike (S) antibodies indeed decline rapidly in the first 3 to 4 months after infection. However, this is followed by a more stable phase between 4- and 8-months after infection with a slower serum anti-S antibody decay rate. The level of serum antibodies correlated with the frequency of S-specific long-lived BMPCs obtained from 18 SARS-CoV-2 convalescent patients 7 to 8 months after i
Abnormal NFκB activation has been implicated in Alzheimer's disease (AD). However, the signaling pathways governing NFκB regulation and function in the brain are poorly understood. We identify complement protein C3 as an astroglial target of NFκB and show that C3 release acts through neuronal C3aR to disrupt dendritic morphology and network function. Exposure to Aβ activates astroglial NFκB and C3 release, consistent with the high levels of C3 expression in brain tissue from AD patients and APP transgenic mice, where C3aR antagonist treatment rescues cognitive impairment. Therefore, dysregulation of neuron-glia interaction through NFκB/C3/C3aR signaling may contribute to synaptic dysfunction in AD, and C3aR antagonists may be therapeutically beneficial.
Small cell lung cancer (SCLC) exists broadly in four molecular subtypes: ASCL1, NEUROD1, POU2F3 and Inflammatory. Initially, SCLC subtypes were thought to be mutually exclusive, but recent evidence shows intra-tumoural subtype heterogeneity and plasticity between subtypes. Here, using a CRISPR-based autochthonous SCLC genetically engineered mouse model to study the consequences of KDM6A/UTX inactivation, we show that KDM6A inactivation induced plasticity from ASCL1 to NEUROD1 resulting in SCLC tumours that express both ASCL1 and NEUROD1. Mechanistically, KDM6A normally maintains an active chromatin state that favours the ASCL1 subtype with its loss decreasing H3K4me1 and increasing H3K27me3 at enhancers of neuroendocrine genes leading to a cell state that is primed for ASCL1-to-NEUROD1 subtype switching. This work identifies KDM6A as an epigenetic regulator that controls ASCL1 to NEUROD1 subtype plasticity and provides an autochthonous SCLC genetically engineered mouse model to model A
KMT2C and KMT2D, encoding histone H3 lysine 4 methyltransferases, are among the most commonly mutated genes in triple-negative breast cancer (TNBC). However, how these mutations may shape epigenomic and transcriptomic landscapes to promote tumorigenesis is largely unknown. Here we describe that deletion of Kmt2c or Kmt2d in non-metastatic murine models of TNBC drives metastasis, especially to the brain. Global chromatin profiling and chromatin immunoprecipitation followed by sequencing revealed altered H3K4me1, H3K27ac and H3K27me3 chromatin marks in knockout cells and demonstrated enhanced binding of the H3K27me3 lysine demethylase KDM6A, which significantly correlated with gene expression. We identified Mmp3 as being commonly upregulated via epigenetic mechanisms in both knockout models. Consistent with these findings, samples from patients with KMT2C-mutant TNBC have higher MMP3 levels. Downregulation or pharmacological inhibition of KDM6A diminished Mmp3 upregulation induced by the
Targeting Excessive EZH1 and EZH2 Activities for Abnormal Histone Methylation and Transcription Network in Mal… MEDIUM▼
Although global H3K27me3 reprogramming is a hallmark of cancer, no effective therapeutic strategy for H3K27me3-high malignancies harboring EZH2WT/WT has yet been established. We explore epigenome and transcriptome in EZH2WT/WT and EZH2WT/Mu aggressive lymphomas and show that mutual interference and compensatory function of co-expressed EZH1 and EZH2 rearrange their own genome-wide distribution, thereby establishing restricted chromatin and gene expression signatures. Direct comparison of leading compounds introduces potency and a mechanism of action of the EZH1/2 dual inhibitor (valemetostat). The synthetic lethality is observed in all lymphoma models and primary adult T cell leukemia-lymphoma (ATL) cells. Opposing actions of EZH1/2-polycomb and SWI/SNF complexes are required for facultative heterochromatin formation. Inactivation of chromatin-associated genes (ARID1A, SMARCA4/BRG1, SMARCB1/SNF5, KDM6A/UTX, BAP1, KMT2D/MLL2) and oncovirus infection (HTLV-1, EBV) trigger EZH1/2 perturba
Wnt-deficient and hypoxic environment orchestrates squamous reprogramming of human pancreatic ductal adenocarc… MEDIUM▼
Human pancreatic cancer is characterized by the molecular diversity encompassing native duct-like and squamous cell-like identities, but mechanisms underlying squamous transdifferentiation have remained elusive. To comprehensively capture the molecular diversity of human pancreatic cancer, we here profiled 65 patient-derived pancreatic cancer organoid lines, including six adenosquamous carcinoma lines. H3K27me3-mediated erasure of the ductal lineage specifiers and hijacking of the TP63-driven squamous-cell programme drove squamous-cell commitment, providing survival benefit in a Wnt-deficient environment and hypoxic conditions. Gene engineering of normal pancreatic duct organoids revealed that GATA6 loss and a Wnt-deficient environment, in concert with genetic or hypoxia-mediated inactivation of KDM6A, facilitate squamous reprogramming, which in turn enhances environmental fitness. EZH2 inhibition counterbalanced the epigenetic bias and curbed the growth of adenosquamous cancer organoi
Anti-CD38 monoclonal antibodies like Daratumumab (Dara) are effective in multiple myeloma (MM); however, drug resistance ultimately occurs and the mechanisms behind this are poorly understood. Here, we identify, via two in vitro genome-wide CRISPR screens probing Daratumumab resistance, KDM6A as an important regulator of sensitivity to Daratumumab-mediated antibody-dependent cellular cytotoxicity (ADCC). Loss of KDM6A leads to increased levels of H3K27me3 on the promoter of CD38, resulting in a marked downregulation in CD38 expression, which may cause resistance to Daratumumab-mediated ADCC. Re-introducing CD38 does not reverse Daratumumab-mediated ADCC fully, which suggests that additional KDM6A targets, including CD48 which is also downregulated upon KDM6A loss, contribute to Daratumumab-mediated ADCC. Inhibition of H3K27me3 with an EZH2 inhibitor resulted in CD38 and CD48 upregulation and restored sensitivity to Daratumumab. These findings suggest KDM6A loss as a mechanism of Daratu
✗ Opposing Evidence 5
Bladder cancer (BC) is a disease that predominantly affects older adults, with aging playing a critical role in its onset and progression. Age-associated phenomena, including immunosenescence and chronic inflammation, form a pro-tumor milieu, while genomic instability and epigenetic drift further increase cancer risk. The review highlights the dual role of DNA methylation in BC: global hypomethylation can activate transposable elements and oncogenes, whereas focal hypermethylation silences tumor-suppressor genes like CDKN2A, especially detrimental in older tissues that rely on these genes for senescence control. In parallel, frequent mutations in chromatin modifiers (e.g., KDM6A, KMT2D) and overexpression of histone-modifying enzymes (e.g., EZH2) alter the tumor epigenome to promote immune evasion and tumor aggressiveness. At the non-coding RNA level, dysregulated microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in BC contribute to aberrant proliferation, metastatic potential, and
Polycomb Repressive Complex 2 (PRC2) establishes H3K27me3 marks to shape spatiotemporal gene expression during embryogenesis. While its dysregulation is linked to developmental disorders, cancer, and aging, the mechanisms guiding PRC2 to specific genomic loci remain a subject of ongoing debate. A prevailing model proposes that PRC2 recruitment occurs via its intrinsic affinity for chromatin rather than through sequence-specific transcription factors. Here, we provide evidence that the maternally deposited pioneer transcription factor Foxh1 plays a critical role in directing PRC2 to specific genomic loci during zygotic genome activation in Xenopus. Foxh1 is a critical transcription factor mediating Nodal signaling, but it also plays an earlier role by pre-binding enhancers prior to signaling activation. This pre-binding is essential for forming enhanceosome complexes that trigger mesendodermal gene expression and drive gastrulation, in cooperation with other maternal transcription facto
H3K36 dimethylation shapes the epigenetic interaction landscape by directing repressive chromatin modification… MEDIUM▼
Epigenetic modifications on the chromatin do not occur in isolation. Chromatin-associated proteins and their modification products form a highly interconnected network, and disturbing one component may rearrange the entire system. We see this increasingly clearly in epigenetically dysregulated cancers. It is important to understand the rules governing epigenetic interactions. Here, we use the mouse embryonic stem cell (mESC) model to describe in detail the relationships within the H3K27-H3K36-DNA methylation subnetwork. In particular, we focus on the major epigenetic reorganization caused by deletion of the histone 3 lysine 36 methyltransferase NSD1, which in mESCs deposits nearly all of the intergenic H3K36me2. Although disturbing the H3K27 and DNA methylation (DNAme) components also affects this network to a certain extent, the removal of H3K36me2 has the most drastic effect on the epigenetic landscape, resulting in full intergenic spread of H3K27me3 and a substantial decrease in DNA
KDM6A loss-of-function mutations in neurodegenerative diseases show progressive cognitive decline despite incr… STRONG▼
Deep learning describes a class of machine learning algorithms that are capable of combining raw inputs into layers of intermediate features. These algorithms have recently shown impressive results across a variety of domains. Biology and medicine are data-rich disciplines, but the data are complex and often ill-understood. Hence, deep learning techniques may be particularly well suited to solve problems of these fields. We examine applications of deep learning to a variety of biomedical problems-patient classification, fundamental biological processes and treatment of patients-and discuss whether deep learning will be able to transform these tasks or if the biomedical sphere poses unique challenges. Following from an extensive literature review, we find that deep learning has yet to revolutionize biomedicine or definitively resolve any of the most pressing challenges in the field, but promising advances have been made on the prior state of the art. Even though improvements over previo
H3K27me3 rejuvenation through KDM6A overexpression fails to rescue age-related neuronal dysfunction in mouse m… MODERATE▼
To evaluate the benefit of adjuvant treatments, such as chemoradiotherapy (CRT) and chemotherapy (CTx), compared with no adjuvant treatment (No-AT) in resected gallbladder (GB) cancer patients, 151 patients were analyzed: 98 (64.9%) patients received adjuvant treatment with CRT (n = 59, 39.1%) or CTx (n = 39, 25.8%), and the remaining 53 (35.1%) did not (No-AT). The clinicopathological factors, patterns of failure, locoregional recurrence-free survival (LRFS), recurrence-free survival (RFS) and overall survival (OS) were compared among the three groups according to tumor stage. In patients with T2-3N0M0 stage disease, the incidences of locoregional recurrence and distant recurrence and 5-year LRFS, RFS and OS rates were not significantly different among the No-AT, CTx, and CRT groups (p > 0.05 each). In those with T2-3N1-2M0 stage disease, the incidences of locoregional recurrence (11.4%, 78.1%, and 68.4%, respectively) and distant recurrence (42.8%, 73.9% and 66.7%, respectively) in t
🧬 Theorist Proposes novel mechanisms and generates creative hypotheses ▼
Novel Therapeutic Hypotheses: Epigenetic Clocks and Neurodegeneration
Hypothesis 1: TET2-Mediated Demethylation Rejuvenation Therapy
Description: Targeted overexpression of TET2 methylcytosine dioxygenase in specific brain regions can reverse pathological DNA methylation patterns associated with accelerated epigenetic aging in neurodegeneration. This approach would restore youthful methylation landscapes at key neuronal survival genes by promoting active demethylation of aberrantly hypermethylated CpG sites.Target: TET2 (Ten-eleven translocation methylcytosine dioxygenase 2)
*
🔍 Skeptic Identifies weaknesses, alternative explanations, and methodological concerns ▼
Critical Evaluation of Epigenetic Clock and Neurodegeneration Hypotheses
Hypothesis 1: TET2-Mediated Demethylation Rejuvenation Therapy
Specific Weaknesses:
Counter-Evidence:
- TET2 overexpression in
🎯 Domain Expert Assesses practical feasibility, druggability, and clinical translation ▼
Druggability Assessment: Epigenetic Clock Neurodegeneration Targets
Overall Assessment Summary
Most hypotheses have fundamental flaws, but I'll assess the top 2-3 for practical drug development feasibility.Hypothesis 2: HDAC3-Selective Inhibition (Revised Confidence: 0.45)
Druggability: MODERATE
Target Class: Zinc metalloenzyme - well-established druggable class Chemical Matter Status: Advanced but limited selectivityExisting Compounds & Clinical Candidates:
- RGFP966 (Repligen): Most selective HDAC3 inhibitor, ~40-fold selectivity over other HDACs
⚖ Synthesizer Integrates perspectives and produces final ranked assessments ▼
Price History
| Event | Price | Change | Source | Time | |
|---|---|---|---|---|---|
| 📄 | New Evidence | $0.418 | ▲ 2.9% | evidence_batch_update | 2026-04-13 02:18 |
| 📄 | New Evidence | $0.406 | ▲ 7.4% | evidence_batch_update | 2026-04-13 02:18 |
| ⚖ | Recalibrated | $0.379 | ▼ 0.5% | 2026-04-12 10:15 | |
| ⚖ | Recalibrated | $0.380 | ▼ 1.5% | 2026-04-10 15:58 | |
| ⚖ | Recalibrated | $0.386 | ▲ 1.7% | 2026-04-10 15:53 | |
| ⚖ | Recalibrated | $0.379 | ▲ 2.7% | 2026-04-08 18:39 | |
| ⚖ | Recalibrated | $0.369 | ▲ 0.9% | 2026-04-06 04:04 | |
| ⚖ | Recalibrated | $0.366 | ▼ 0.9% | 2026-04-04 16:38 | |
| ⚖ | Recalibrated | $0.369 | ▼ 3.9% | 2026-04-04 16:02 | |
| 📄 | New Evidence | $0.384 | ▲ 4.5% | evidence_batch_update | 2026-04-04 09:08 |
| ⚖ | Recalibrated | $0.368 | ▼ 6.6% | 2026-04-03 23:46 | |
| ⚖ | Recalibrated | $0.394 | ▲ 4.4% | 2026-04-02 21:55 | |
| ⚖ | Recalibrated | $0.378 | ▼ 5.5% | market_recalibrate | 2026-04-02 19:14 |
| 💬 | Debate Round | $0.399 | ▲ 2.5% | debate_engine | 2026-04-02 17:18 |
| 📄 | New Evidence | $0.389 | ▼ 10.0% | market_dynamics | 2026-04-02 17:18 |
Clinical Trials (10) Relevance: 66%
Active
Completed
Total Enrolled
Highest Phase
📚 Cited Papers (44)
📓 Linked Notebooks (1)
Wiki Pages
KG Entities (42)
Dependency Graph (0 upstream, 2 downstream)
Linked Experiments (6)
Related Hypotheses
Estimated Development
🧪 Falsifiable Predictions (1)
Knowledge Subgraph (98 edges)
activates (1)
associated with (5)
co associated with (15)
deacetylates (1)
implicated in (6)
methylates (1)
participates in (5)
predicts (1)
regulated by (1)
requires (1)
Mechanism Pathway for KDM6A
Molecular pathway showing key causal relationships underlying this hypothesis
graph TD
KDM6A["KDM6A"] -->|demethylates| H3K27me3["H3K27me3"]
KDM6A_1["KDM6A"] -->|associated with| neurodegeneration["neurodegeneration"]
HDAC3["HDAC3"] -->|co discussed| KDM6A_2["KDM6A"]
TET2["TET2"] -->|co discussed| KDM6A_3["KDM6A"]
KDM6A_4["KDM6A"] -->|co discussed| SIRT6["SIRT6"]
KDM6A_5["KDM6A"] -->|co discussed| DNMT1["DNMT1"]
KDM6A_6["KDM6A"] -->|co discussed| FOXO3["FOXO3"]
DNMT1_7["DNMT1"] -->|co discussed| KDM6A_8["KDM6A"]
SIRT6_9["SIRT6"] -->|co discussed| KDM6A_10["KDM6A"]
KDM6A_11["KDM6A"] -->|co discussed| TET2_12["TET2"]
FOXO3_13["FOXO3"] -->|co discussed| KDM6A_14["KDM6A"]
KDM6A_15["KDM6A"] -->|co discussed| HDAC3_16["HDAC3"]
DNMT1_17["DNMT1"] -->|co associated with| KDM6A_18["KDM6A"]
HDAC3_19["HDAC3"] -->|co associated with| KDM6A_20["KDM6A"]
KDM6A_21["KDM6A"] -->|co associated with| TET2_22["TET2"]
style KDM6A fill:#ce93d8,stroke:#333,color:#000
style H3K27me3 fill:#4fc3f7,stroke:#333,color:#000
style KDM6A_1 fill:#ce93d8,stroke:#333,color:#000
style neurodegeneration fill:#ef5350,stroke:#333,color:#000
style HDAC3 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_2 fill:#ce93d8,stroke:#333,color:#000
style TET2 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_3 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_4 fill:#ce93d8,stroke:#333,color:#000
style SIRT6 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_5 fill:#ce93d8,stroke:#333,color:#000
style DNMT1 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_6 fill:#ce93d8,stroke:#333,color:#000
style FOXO3 fill:#ce93d8,stroke:#333,color:#000
style DNMT1_7 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_8 fill:#ce93d8,stroke:#333,color:#000
style SIRT6_9 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_10 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_11 fill:#ce93d8,stroke:#333,color:#000
style TET2_12 fill:#ce93d8,stroke:#333,color:#000
style FOXO3_13 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_14 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_15 fill:#ce93d8,stroke:#333,color:#000
style HDAC3_16 fill:#ce93d8,stroke:#333,color:#000
style DNMT1_17 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_18 fill:#ce93d8,stroke:#333,color:#000
style HDAC3_19 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_20 fill:#ce93d8,stroke:#333,color:#000
style KDM6A_21 fill:#ce93d8,stroke:#333,color:#000
style TET2_22 fill:#ce93d8,stroke:#333,color:#000
3D Protein Structure
🧬 KDM6A — PDB 3AVR Click to expand 3D viewer
Source Analysis
Epigenetic clocks and biological aging in neurodegeneration
neurodegeneration | 2026-04-01 | completed