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## Question

# Gene Research for Functional Annotation

## ⚠️ CRITICAL: Gene/Protein Identification Context

**BEFORE YOU BEGIN RESEARCH:** You MUST verify you are researching the CORRECT gene/protein. Gene symbols can be ambiguous, especially for less well-characterized genes from non-model organisms.

### Target Gene/Protein Identity (from UniProt):
- **UniProt Accession:** Q9NY61
- **Protein Description:** RecName: Full=Protein AATF; AltName: Full=Apoptosis-antagonizing transcription factor; AltName: Full=Rb-binding protein Che-1;
- **Gene Information:** Name=AATF {ECO:0000312|HGNC:HGNC:19235}; Synonyms=CHE1, DED; ORFNames=HSPC277;
- **Organism (full):** Homo sapiens (Human).
- **Protein Family:** Belongs to the AATF family. .
- **Key Domains:** AATF. (IPR025160); AATF/Bfr2. (IPR039223); AATF_C. (IPR012617); AATF-Che1 (PF13339); TRAUB (PF08164)

### MANDATORY VERIFICATION STEPS:

1. **Check if the gene symbol "AATF" matches the protein description above**
2. **Verify the organism is correct:** Homo sapiens (Human).
3. **Check if protein family/domains align with what you find in literature**
4. **If you find literature for a DIFFERENT gene with the same or similar symbol, STOP**

### If Gene Symbol is Ambiguous or You Cannot Find Relevant Literature:

**DO NOT PROCEED WITH RESEARCH ON A DIFFERENT GENE.** Instead:
- State clearly: "The gene symbol 'AATF' is ambiguous or literature is limited for this specific protein"
- Explain what you found (e.g., "Found extensive literature on a different gene with the same symbol in a different organism")
- Describe the protein based ONLY on the UniProt information provided above
- Suggest that the protein function can be inferred from domain/family information

### Research Target:

Please provide a comprehensive research report on the gene **AATF** (gene ID: AATF, UniProt: Q9NY61) in human.

The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.

You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.

We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.

We are interested in where in or outside the cell the gene product carries out its function.

We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.

Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.

## Output

Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on:
1. Key concepts and definitions with current understanding
2. Recent developments and latest research (prioritize 2023-2024 sources)
3. Current applications and real-world implementations
4. Expert opinions and analysis from authoritative sources
5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available.
Always prioritize recent, authoritative sources and provide specific citations for all major claims.

# Gene Research for Functional Annotation

## ⚠️ CRITICAL: Gene/Protein Identification Context

**BEFORE YOU BEGIN RESEARCH:** You MUST verify you are researching the CORRECT gene/protein. Gene symbols can be ambiguous, especially for less well-characterized genes from non-model organisms.

### Target Gene/Protein Identity (from UniProt):
- **UniProt Accession:** Q9NY61
- **Protein Description:** RecName: Full=Protein AATF; AltName: Full=Apoptosis-antagonizing transcription factor; AltName: Full=Rb-binding protein Che-1;
- **Gene Information:** Name=AATF {ECO:0000312|HGNC:HGNC:19235}; Synonyms=CHE1, DED; ORFNames=HSPC277;
- **Organism (full):** Homo sapiens (Human).
- **Protein Family:** Belongs to the AATF family. .
- **Key Domains:** AATF. (IPR025160); AATF/Bfr2. (IPR039223); AATF_C. (IPR012617); AATF-Che1 (PF13339); TRAUB (PF08164)

### MANDATORY VERIFICATION STEPS:

1. **Check if the gene symbol "AATF" matches the protein description above**
2. **Verify the organism is correct:** Homo sapiens (Human).
3. **Check if protein family/domains align with what you find in literature**
4. **If you find literature for a DIFFERENT gene with the same or similar symbol, STOP**

### If Gene Symbol is Ambiguous or You Cannot Find Relevant Literature:

**DO NOT PROCEED WITH RESEARCH ON A DIFFERENT GENE.** Instead:
- State clearly: "The gene symbol 'AATF' is ambiguous or literature is limited for this specific protein"
- Explain what you found (e.g., "Found extensive literature on a different gene with the same symbol in a different organism")
- Describe the protein based ONLY on the UniProt information provided above
- Suggest that the protein function can be inferred from domain/family information

### Research Target:

Please provide a comprehensive research report on the gene **AATF** (gene ID: AATF, UniProt: Q9NY61) in human.

The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.

You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.

We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.

We are interested in where in or outside the cell the gene product carries out its function.

We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.

Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.

## Research report: Human **AATF / Che-1** (UniProt **Q9NY61**) — functional annotation, pathways, localization, and translational relevance

### Executive summary
AATF (apoptosis-antagonizing transcription factor; also known as Che-1) is a non-enzymatic transcriptional regulator described as an RNA polymerase I/II-binding protein that functions primarily in the nucleus/nucleolus, linking transcription programs to cell-cycle control, apoptosis resistance, nucleolar/ribosome-related programs, and stress responses including DNA damage response. Recent work highlights two mechanistically detailed disease contexts: (i) glioblastoma, where AATF cooperates with NRF-1 to maintain mitochondrial oxidative phosphorylation (OXPHOS) gene expression and tumor proliferation, and (ii) multiple myeloma, where Che-1/AATF connects to Hippo pathway effector TAZ through a miR-590-3p axis with implications for bone disease and liquid-biopsy/therapeutic strategies. (sorino2026aatfsupportsproliferation pages 1-4, sorino2026aatfsupportsproliferation pages 22-25, bruno2024molecularinsightsunlocking pages 2-4)

### 1) Key concepts and definitions (current understanding)

#### 1.1 Target verification (identity and synonyms)
The human gene/protein in scope is **AATF**, synonymous with **Che-1** and explicitly expanded in the literature as **“Che-1/Apoptosis Antagonising Transcription Factor (AATF)”**. It is described as an **RNA polymerase (RNA Pol) I and II binding protein** mainly involved in transcriptional regulation. (sorino2026aatfsupportsproliferation pages 1-4)

#### 1.2 Functional class: transcriptional regulator (not a catalytic enzyme)
AATF/Che-1 is presented as a **transcriptional regulator/cofactor**, rather than an enzyme or transporter, operating by binding transcriptional machinery and cooperating with transcription factors to shape gene expression programs involved in proliferation, survival, and stress responses. (sorino2026aatfsupportsproliferation pages 1-4, sorino2026aatfsupportsproliferation pages 19-22)

#### 1.3 Subcellular localization (where AATF acts)
AATF is reported as **predominantly nuclear and nucleolar**, with additional detection in other compartments (e.g., cytoplasm/mitochondria in some contexts), consistent with its dual linkage to RNA Pol II transcription (nucleus/chromatin) and RNA Pol I–associated programs (nucleolus). (sorino2026aatfsupportsproliferation pages 4-8, sorino2026aatfsupportsproliferation pages 22-25)

### 2) Molecular functions, pathways, and mechanisms

#### 2.1 RNA polymerase I and ribosome/nucleolar function
AATF/Che-1 is reported to **bind RNA polymerase I machinery and sustain ribosomal RNA gene transcription**, supporting a role in nucleolar function and ribosome biogenesis-related transcription. (sorino2026aatfsupportsproliferation pages 22-25)

#### 2.2 RNA polymerase II transcriptional cofactor activity (NRF-1/OXPHOS program)
A detailed mechanistic model in glioblastoma positions AATF as an NRF-1-associated transcriptional cofactor:

- AATF **physically interacts with NRF-1** and is required for **NRF-1-mediated transcription** of nuclear-encoded OXPHOS genes by affecting **RNA polymerase II recruitment** and chromatin state. (sorino2026aatfsupportsproliferation pages 1-4, sorino2026aatfsupportsproliferation pages 19-22)
- AATF occupancy at OXPHOS promoters is linked to NRF-1 motifs and productive transcription depends on AATF, consistent with a co-activator/cofactor role for Pol II-dependent expression programs. (sorino2026aatfsupportsproliferation pages 19-22)

#### 2.3 DNA damage response and stress signaling (p53-linked DDR)
AATF is described as an important mediator of the **p53-driven DNA damage response**, with stress-dependent regulation via DDR kinases (e.g., MK2/ATM/CHK2) and multiple post-translational modifications (phosphorylation, PARylation, ubiquitination, isomerization). These regulatory layers provide a mechanistic rationale for why AATF frequently associates with survival and therapy resistance phenotypes in cancer contexts. (bredow2025zudenmechanismen pages 19-21)

### 3) Recent developments and latest research (prioritize 2023–2024)

#### 3.1 2024: Che-1/AATF–Hippo/TAZ crosstalk in multiple myeloma (MM)
A 2024 commentary/review highlights Che-1/AATF as an **RNA polymerase binding factor** implicated in MM progression and introduces a mechanistic crosstalk with Hippo signaling:

- Che-1/AATF promotes transcription of **miR-590-3p**, which in turn downregulates **TAZ** (Hippo effector) in mesenchymal/adipose-derived stem cells, inhibiting osteoblastogenesis/mineralization; in a Vk*Che-1 model this is associated with **increased bone resorption and decreased bone formation**. (bruno2024molecularinsightsunlocking pages 2-4, bruno2024molecularinsightsunlocking pages 1-2)
- Translational ideas proposed include **detecting miR-590-3p in liquid biopsy**, suppressing miR-590-3p using RNA-inhibitor nanocomplexes, and combining with approaches (e.g., demethylating agents) aimed at restoring TAZ function. (bruno2024molecularinsightsunlocking pages 2-4, bruno2024molecularinsightsunlocking pages 1-2)

This work provides an updated (2024) conceptual model for how a tumor-intrinsic transcriptional regulator (Che-1/AATF) can drive microenvironmental pathology (bone disease) through secreted miRNA signaling. (bruno2024molecularinsightsunlocking pages 2-4)

### 4) Current applications and real-world implementations

#### 4.1 Biomarker/prognostic applications (glioblastoma)
In glioblastoma datasets, AATF is upregulated in tumor vs non-tumor tissue and high AATF expression associates with worse overall survival, supporting AATF as a **candidate prognostic biomarker** in GBM. This is shown visually in a figure containing expression comparisons (Rembrandt and Gravendeel) and a Kaplan–Meier survival curve linking higher AATF to poorer survival. (sorino2026aatfsupportsproliferation media 597740c9)

#### 4.2 Therapeutic targeting strategies (conceptual and preclinical)
- **Glioblastoma**: AATF knockdown produces proliferation arrest and increases sensitivity to temozolomide in cell models, consistent with AATF as a **therapy-sensitizing target** conceptually, particularly given links to DNA repair programs (e.g., downregulation of base excision repair on AATF depletion). (sorino2026aatfsupportsproliferation pages 22-25, sorino2026aatfsupportsproliferation pages 12-16)
- **Multiple myeloma**: The Che-1–miR-590-3p–TAZ axis suggests actionable points (miRNA detection/inhibition; restoring TAZ), and the commentary explicitly frames these as routes to “unlock therapeutic potential” in MM and bone disease. (bruno2024molecularinsightsunlocking pages 2-4, bruno2024molecularinsightsunlocking pages 1-2)

A key practical limitation emphasized in the GBM-focused primary study is that **no compounds capable of directly inhibiting AATF activity** were identified in their discussion, and a lack of structural information complicates inhibitor discovery. (sorino2026aatfsupportsproliferation pages 22-25)

### 5) Expert opinions/analysis from authoritative sources (within retrieved evidence)

#### 5.1 Multiple myeloma viewpoint (2024 expert commentary)
The 2024 article explicitly interprets Che-1/AATF as a protein “which has emerged as a potential player” in myeloma cell survival/proliferation and frames the Che-1/TAZ crosstalk as an emerging set of “new molecular targets” to limit MM proliferation and bone lesions. (bruno2024molecularinsightsunlocking pages 1-2)

#### 5.2 Glioblastoma viewpoint (mechanistic primary research)
The glioblastoma study interprets AATF as a central transcriptional cofactor supporting tumor proliferation by maintaining mitochondrial respiration via NRF-1-dependent OXPHOS transcription, and frames AATF as having therapeutic-target potential while noting the present lack of direct inhibitors. (sorino2026aatfsupportsproliferation pages 19-22, sorino2026aatfsupportsproliferation pages 22-25, sorino2026aatfsupportsproliferation pages 1-4)

### 6) Relevant statistics and data (from recent studies in this run)

#### 6.1 Glioblastoma (expression, prognosis, and mechanistic quantitative readouts)
- Patient datasets used for AATF expression comparisons include Rembrandt **GBM n=219 vs non-tumour n=28** and Gravendeel **GBM n=159 vs non-tumour n=8**, with high AATF linked to poorer survival by Kaplan–Meier (visual evidence). (sorino2026aatfsupportsproliferation pages 12-16, sorino2026aatfsupportsproliferation media 597740c9)
- Transcriptome impact of AATF depletion in GBM: **2,427 genes** modulated (1,258 up; 1,169 down; q<0.05, |log2FC|>0.7), and **53/66 OXPHOS signature genes** downregulated. (sorino2026aatfsupportsproliferation pages 16-19)
- Patient-level correlation reported between AATF and NRF-1 expression: **R=0.52, p=1.3×10⁻¹²**. (sorino2026aatfsupportsproliferation pages 16-19)

#### 6.2 Multiple myeloma (cohort size and epidemiologic statistics)
- The 2024 MM commentary references CoMMpass cohort expression analyses with **N=687** patients. (bruno2024molecularinsightsunlocking pages 2-4)
- MM burden statistics cited in the same source: MM accounts for approximately **10–15% of hematologic cancers** and **~20% of cancer-related deaths**. (bruno2024molecularinsightsunlocking pages 1-2)

### Evidence synthesis table
The following table compiles evidence-supported functional annotation areas, mechanisms, localizations, and translational notes.

| Functional area | Key mechanistic role | Subcellular localization | Evidence/data points | Representative recent source (year, journal) with URL | Notes on applications/implications |
|---|---|---|---|---|---|
| Gene/protein identity | Human AATF is the same protein as Che-1 / apoptosis-antagonizing transcription factor; described as an RNA polymerase I and II binding transcriptional regulator | Predominantly nuclear and nucleolar; additional reports of centrosomal, Golgi, cytoplasmic, and mitochondrial detection | Multiple extracted snippets explicitly equate AATF with Che-1 and describe nuclear/nucleolar localization and RNA polymerase-binding function (sorino2026aatfsupportsproliferation pages 4-8, sorino2026aatfsupportsproliferation pages 1-4, bredow2025zudenmechanismen pages 19-21) | Sorino et al., 2026, *Cell Death & Disease* — https://doi.org/10.1038/s41419-026-08617-0 | Confirms that the literature aligns with UniProt Q9NY61 human AATF/Che-1 rather than an unrelated gene/protein |
| Transcriptional regulation | Acts as a transcriptional regulator/cofactor interacting with transcription factors and regulatory proteins; supports RNA polymerase II recruitment to target genes | Nuclear/chromatin-associated; nucleolar for RNA Pol I-linked functions | AATF is described as mainly involved in transcriptional regulation and required for NRF-1-mediated transcription of OXPHOS genes by affecting RNA Pol II recruitment and chromatin structure (sorino2026aatfsupportsproliferation pages 1-4, sorino2026aatfsupportsproliferation pages 19-22) | Sorino et al., 2026, *Cell Death & Disease* — https://doi.org/10.1038/s41419-026-08617-0 | Positions AATF as a non-enzymatic regulatory factor rather than a catalytic protein; suggests vulnerability at the level of transcriptional complexes |
| Ribosome biogenesis / nucleolar function | Binds RNA polymerase I machinery and sustains ribosomal RNA gene transcription, linking AATF to nucleolar function and ribosome biogenesis | Nucleolus and nucleus | Extracted evidence states Che-1/AATF binds RNA polymerase I machinery and sustains rRNA gene transcription; this is consistent with nucleolar localization claims (sorino2026aatfsupportsproliferation pages 22-25) | Sorino et al., 2026, *Cell Death & Disease* — https://doi.org/10.1038/s41419-026-08617-0 | Supports annotation of AATF as a nucleolar regulator of ribosome production and nucleolar homeostasis, relevant to proliferative disease states |
| DNA damage response / p53-linked stress signaling | Mediator of p53-driven DNA damage response; activated by DDR kinases (MK2, ATM, CHK2) and regulated by phosphorylation, PARylation, ubiquitination, and isomerization; PARP1 stabilizes AATF during damage | Primarily nuclear; stress-responsive | Extracted evidence identifies AATF as an important mediator of the cellular response to p53-driven DDR and details stress-induced post-translational regulation (bredow2025zudenmechanismen pages 19-21) | Bredow, 2025, unknown journal/thesis source — no validated journal URL extracted; supporting identity/DDR details also summarized in Sorino et al., 2026, *Cell Death & Disease* — https://doi.org/10.1038/s41419-026-08617-0 | Mechanistically links AATF to survival after genotoxic stress and helps explain why AATF can contribute to therapy resistance |
| Apoptosis and cell-cycle control | Anti-apoptotic factor that modulates cell-cycle and stress-response genes; linked to Rb-mediated growth suppression pathways | Nuclear/nucleolar | Extracted evidence states AATF mediates anti-apoptotic effects and influences cell-cycle control, including interaction with RNA polymerase II subunit 11 and effects on Rb-mediated growth suppression (sorino2026aatfsupportsproliferation pages 22-25, bredow2025zudenmechanismen pages 19-21) | Sorino et al., 2026, *Cell Death & Disease* — https://doi.org/10.1038/s41419-026-08617-0 | Explains why AATF is recurrently associated with tumor cell survival and proliferation |
| Mitochondrial respiration / GBM biology | Interacts with NRF-1 and is essential for NRF-1-dependent transcription of nuclear-encoded OXPHOS genes; promotes mitochondrial respiration and GBM proliferation | Nuclear/chromatin-associated for transcriptional mechanism; mitochondrial phenotype observed downstream | RNA-seq after AATF silencing modulated 2,427 genes (1,258 up, 1,169 down); 53/66 OXPHOS-signature genes were downregulated; AATF and NRF-1 expression correlated in GBM patients (R=0.52, p=1.3e-12); AATF loss reduced OCR and ATP, increased mitochondrial ROS, altered morphology, and reduced colony formation/tumorigenicity (sorino2026aatfsupportsproliferation pages 16-19, sorino2026aatfsupportsproliferation pages 12-16) | Sorino et al., 2026, *Cell Death & Disease* — https://doi.org/10.1038/s41419-026-08617-0 | Provides a concrete, disease-relevant functional annotation for AATF in cancer metabolism; suggests AATF as a GBM therapeutic target |
| Clinical expression/prognosis in GBM | Upregulated in glioblastoma and associated with poorer overall survival | Tumor tissue-level observation | Rembrandt dataset: GBM n=219 vs non-tumor n=28; Gravendeel dataset: GBM n=159 vs non-tumor n=8; Kaplan–Meier analysis showed poorer survival with high AATF expression; figure evidence confirms significant upregulation and adverse survival association (sorino2026aatfsupportsproliferation pages 12-16, sorino2026aatfsupportsproliferation media 597740c9) | Sorino et al., 2026, *Cell Death & Disease* — https://doi.org/10.1038/s41419-026-08617-0 | Supports translational use of AATF as a prognostic biomarker candidate in GBM |
| Therapy response / DNA repair in GBM | Supports DNA repair programs and contributes to resistance to temozolomide and chemoradiotherapy; depletion sensitizes cells | Nuclear/chromatin-associated | Extracted evidence notes downregulation of base excision repair upon AATF loss and increased sensitivity to temozolomide; cited linked work reports AATF promotes efficient DNA repair in glioblastoma stem cells (sorino2026aatfsupportsproliferation pages 19-22, sorino2026aatfsupportsproliferation pages 22-25, sorino2026aatfsupportsproliferation pages 12-16) | Sorino et al., 2026, *Cell Death & Disease* — https://doi.org/10.1038/s41419-026-08617-0 | Indicates AATF could be explored as a therapy-sensitizing target, especially in DNA-damaging treatment settings |
| Multiple myeloma / Hippo-TAZ crosstalk | Che-1/AATF promotes miR-590-3p expression, which suppresses TAZ in bone niche cells; this links tumor-intrinsic Che-1 activity to osteoblastogenesis defects and bone disease | Transcriptional role in MM cells; microenvironmental effects in mesenchymal/adipose-derived stem cells | Che-1 overexpression promoted miR-590-3p release; miR-590-3p downregulated TAZ and inhibited osteoblastogenesis/mineralization; in Vk*Che-1 mice this associated with increased bone resorption and decreased bone formation; CoMMpass cohort size reported as N=687 (bruno2024molecularinsightsunlocking pages 2-4, bruno2024molecularinsightsunlocking pages 1-2) | Bruno et al., 2024, *Journal of Experimental & Clinical Cancer Research* — https://doi.org/10.1186/s13046-024-03248-9 | Extends functional annotation beyond cell-autonomous survival to tumor–microenvironment signaling; highlights the Che-1–miR-590-3p–TAZ axis as a translational target in MM bone disease |
| Therapeutic tractability / current limitations | AATF is proposed as a therapeutic target, but no direct inhibitors or 3D structure were identified in the extracted evidence | Not applicable | Extracted evidence explicitly states no compounds capable of inhibiting AATF activity had been identified and lack of a 3D structure complicates inhibitor discovery; MM commentary mentions exploratory strategies such as liquid-biopsy miR-590-3p detection, RNA inhibitor nanocomplexes, demethylating agents to restore TAZ, and reported Che-1 antagonist Marimastat in other work (bruno2024molecularinsightsunlocking pages 2-4, sorino2026aatfsupportsproliferation pages 22-25, sorino2026aatfsupportsproliferation pages 1-4) | Bruno et al., 2024, *J Exp Clin Cancer Res* — https://doi.org/10.1186/s13046-024-03248-9; Sorino et al., 2026, *Cell Death & Disease* — https://doi.org/10.1038/s41419-026-08617-0 | Most immediate real-world relevance is biomarker development and pathway-targeted combination strategies rather than established direct AATF inhibition |


*Table: This table summarizes evidence-supported functional annotation for human AATF/Che-1, emphasizing identity, localization, molecular mechanisms, disease relevance, and translational implications. It is restricted to findings explicitly supported by the extracted evidence in this session.*

### Reference details (URLs and publication dates)
- Bruno T, et al. **“Molecular insights unlocking therapeutic potential for multiple myeloma and bone disease management.”** *Journal of Experimental & Clinical Cancer Research* (publication month/year: **Dec 2024**). DOI URL: https://doi.org/10.1186/s13046-024-03248-9 (bruno2024molecularinsightsunlocking pages 2-4, bruno2024molecularinsightsunlocking pages 1-2)
- Sorino C, et al. **“AATF supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an NRF-1-dependent mechanism.”** *Cell Death & Disease* (publication month/year: **Mar 2026**). DOI URL: https://doi.org/10.1038/s41419-026-08617-0 (sorino2026aatfsupportsproliferation pages 1-4, sorino2026aatfsupportsproliferation pages 16-19)

### Scope note and limitations
This report is constrained to sources successfully retrieved and evidence-extracted in this session. While it includes an authoritative 2024 MM-focused commentary and mechanistically detailed GBM primary data, additional 2023–2024 primary studies dedicated specifically to AATF’s nucleolar/ribosome and DNA-damage roles likely exist but were not captured in the current retrieval set; claims here are therefore limited to what is directly supported by the cited evidence. (sorino2026aatfsupportsproliferation pages 22-25, bredow2025zudenmechanismen pages 19-21, bruno2024molecularinsightsunlocking pages 1-2)

References

1. (sorino2026aatfsupportsproliferation pages 1-4): Cristina Sorino, Stefano Di Giovenale, Italia Falcone, Francesca Romana Auciello, Claudio Pulito, Federica Lo Sardo, Stefano Scalera, Francesca De Nicola, Valeria Catena, Ludovica Ciuffreda, Brindusa Ana Maria Arteni, Stefano Giuliani, Bruno Amadio, Giovanni Blandino, Maurizio Fanciulli, and Simona Iezzi. Aatf supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an nrf-1-dependent mechanism. Cell Death &amp; Disease, Mar 2026. URL: https://doi.org/10.1038/s41419-026-08617-0, doi:10.1038/s41419-026-08617-0. This article has 0 citations and is from a peer-reviewed journal.

2. (sorino2026aatfsupportsproliferation pages 22-25): Cristina Sorino, Stefano Di Giovenale, Italia Falcone, Francesca Romana Auciello, Claudio Pulito, Federica Lo Sardo, Stefano Scalera, Francesca De Nicola, Valeria Catena, Ludovica Ciuffreda, Brindusa Ana Maria Arteni, Stefano Giuliani, Bruno Amadio, Giovanni Blandino, Maurizio Fanciulli, and Simona Iezzi. Aatf supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an nrf-1-dependent mechanism. Cell Death &amp; Disease, Mar 2026. URL: https://doi.org/10.1038/s41419-026-08617-0, doi:10.1038/s41419-026-08617-0. This article has 0 citations and is from a peer-reviewed journal.

3. (bruno2024molecularinsightsunlocking pages 2-4): Tiziana Bruno, Valeria Catena, Giovanni Blandino, Maurizio Fanciulli, and Silvia Di Agostino. Molecular insights unlocking therapeutic potential for multiple myeloma and bone disease management. Journal of Experimental & Clinical Cancer Research : CR, Dec 2024. URL: https://doi.org/10.1186/s13046-024-03248-9, doi:10.1186/s13046-024-03248-9. This article has 2 citations.

4. (sorino2026aatfsupportsproliferation pages 19-22): Cristina Sorino, Stefano Di Giovenale, Italia Falcone, Francesca Romana Auciello, Claudio Pulito, Federica Lo Sardo, Stefano Scalera, Francesca De Nicola, Valeria Catena, Ludovica Ciuffreda, Brindusa Ana Maria Arteni, Stefano Giuliani, Bruno Amadio, Giovanni Blandino, Maurizio Fanciulli, and Simona Iezzi. Aatf supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an nrf-1-dependent mechanism. Cell Death &amp; Disease, Mar 2026. URL: https://doi.org/10.1038/s41419-026-08617-0, doi:10.1038/s41419-026-08617-0. This article has 0 citations and is from a peer-reviewed journal.

5. (sorino2026aatfsupportsproliferation pages 4-8): Cristina Sorino, Stefano Di Giovenale, Italia Falcone, Francesca Romana Auciello, Claudio Pulito, Federica Lo Sardo, Stefano Scalera, Francesca De Nicola, Valeria Catena, Ludovica Ciuffreda, Brindusa Ana Maria Arteni, Stefano Giuliani, Bruno Amadio, Giovanni Blandino, Maurizio Fanciulli, and Simona Iezzi. Aatf supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an nrf-1-dependent mechanism. Cell Death &amp; Disease, Mar 2026. URL: https://doi.org/10.1038/s41419-026-08617-0, doi:10.1038/s41419-026-08617-0. This article has 0 citations and is from a peer-reviewed journal.

6. (bredow2025zudenmechanismen pages 19-21): J Bredow. Zu den mechanismen der nierendegeneration durch die akkumulation von dna-schäden und r-loops. Unknown journal, 2025.

7. (bruno2024molecularinsightsunlocking pages 1-2): Tiziana Bruno, Valeria Catena, Giovanni Blandino, Maurizio Fanciulli, and Silvia Di Agostino. Molecular insights unlocking therapeutic potential for multiple myeloma and bone disease management. Journal of Experimental & Clinical Cancer Research : CR, Dec 2024. URL: https://doi.org/10.1186/s13046-024-03248-9, doi:10.1186/s13046-024-03248-9. This article has 2 citations.

8. (sorino2026aatfsupportsproliferation media 597740c9): Cristina Sorino, Stefano Di Giovenale, Italia Falcone, Francesca Romana Auciello, Claudio Pulito, Federica Lo Sardo, Stefano Scalera, Francesca De Nicola, Valeria Catena, Ludovica Ciuffreda, Brindusa Ana Maria Arteni, Stefano Giuliani, Bruno Amadio, Giovanni Blandino, Maurizio Fanciulli, and Simona Iezzi. Aatf supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an nrf-1-dependent mechanism. Cell Death &amp; Disease, Mar 2026. URL: https://doi.org/10.1038/s41419-026-08617-0, doi:10.1038/s41419-026-08617-0. This article has 0 citations and is from a peer-reviewed journal.

9. (sorino2026aatfsupportsproliferation pages 12-16): Cristina Sorino, Stefano Di Giovenale, Italia Falcone, Francesca Romana Auciello, Claudio Pulito, Federica Lo Sardo, Stefano Scalera, Francesca De Nicola, Valeria Catena, Ludovica Ciuffreda, Brindusa Ana Maria Arteni, Stefano Giuliani, Bruno Amadio, Giovanni Blandino, Maurizio Fanciulli, and Simona Iezzi. Aatf supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an nrf-1-dependent mechanism. Cell Death &amp; Disease, Mar 2026. URL: https://doi.org/10.1038/s41419-026-08617-0, doi:10.1038/s41419-026-08617-0. This article has 0 citations and is from a peer-reviewed journal.

10. (sorino2026aatfsupportsproliferation pages 16-19): Cristina Sorino, Stefano Di Giovenale, Italia Falcone, Francesca Romana Auciello, Claudio Pulito, Federica Lo Sardo, Stefano Scalera, Francesca De Nicola, Valeria Catena, Ludovica Ciuffreda, Brindusa Ana Maria Arteni, Stefano Giuliani, Bruno Amadio, Giovanni Blandino, Maurizio Fanciulli, and Simona Iezzi. Aatf supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an nrf-1-dependent mechanism. Cell Death &amp; Disease, Mar 2026. URL: https://doi.org/10.1038/s41419-026-08617-0, doi:10.1038/s41419-026-08617-0. This article has 0 citations and is from a peer-reviewed journal.

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2. sorino2026aatfsupportsproliferation pages 22-25
3. sorino2026aatfsupportsproliferation pages 19-22
4. bredow2025zudenmechanismen pages 19-21
5. bruno2024molecularinsightsunlocking pages 2-4
6. bruno2024molecularinsightsunlocking pages 1-2
7. sorino2026aatfsupportsproliferation pages 16-19
8. sorino2026aatfsupportsproliferation pages 4-8
9. sorino2026aatfsupportsproliferation pages 12-16
10. https://doi.org/10.1038/s41419-026-08617-0
11. https://doi.org/10.1186/s13046-024-03248-9
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13. https://doi.org/10.1038/s41419-026-08617-0,
14. https://doi.org/10.1186/s13046-024-03248-9,