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protein_family: Belongs to the bZIP family. ATF subfamily. .
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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: Q20435
• Protein Description: RecName: Full=Transcription factor atf-6 homolog {ECO:0000303|PubMed:16184190}; AltName: Full=Cyclic AMP-dependent transcription factor ATF-6 homolog {ECO:0000305};
• Gene Information: Name=atf-6 {ECO:0000312|WormBase:F45E6.2}; ORFNames=F45E6.2 {ECO:0000312|WormBase:F45E6.2};
• Organism (full): Caenorhabditis elegans.
• Protein Family: Belongs to the bZIP family. ATF subfamily. .
• Key Domains: ATF_bZIP_TF. (IPR051882); bZIP. (IPR004827); bZIP_sf. (IPR046347); bZIP_2 (PF07716)

MANDATORY VERIFICATION STEPS:

1. Check if the gene symbol "atf-6" matches the protein description above
2. Verify the organism is correct: Caenorhabditis elegans.
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 'atf-6' 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 atf-6 (gene ID: atf-6, UniProt: Q20435) in worm.

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this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.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: Q20435
• Protein Description: RecName: Full=Transcription factor atf-6 homolog {ECO:0000303|PubMed:16184190}; AltName: Full=Cyclic AMP-dependent transcription factor ATF-6 homolog {ECO:0000305};
• Gene Information: Name=atf-6 {ECO:0000312|WormBase:F45E6.2}; ORFNames=F45E6.2 {ECO:0000312|WormBase:F45E6.2};
• Organism (full): Caenorhabditis elegans.
• Protein Family: Belongs to the bZIP family. ATF subfamily. .
• Key Domains: ATF_bZIP_TF. (IPR051882); bZIP. (IPR004827); bZIP_sf. (IPR046347); bZIP_2 (PF07716)

MANDATORY VERIFICATION STEPS:

1. Check if the gene symbol "atf-6" matches the protein description above
2. Verify the organism is correct: Caenorhabditis elegans.
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 'atf-6' 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 atf-6 (gene ID: atf-6, UniProt: Q20435) in worm.

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 plan status
- Objective 1 (identity verification): Completed. The target is atf-6 (locus F45E6.2) from Caenorhabditis elegans, UniProt Q20435; a bZIP transcription factor of the ATF subfamily, consistent with an ER stress sensor in the UPR. No conflicting gene symbol usage detected.
- Objective 2 (literature gathering): Completed. Key sources include Burkewitz et al., 2020 (Cell Reports), Waldherr et al., 2019 (Nature Communications), Beaudoin‑Chabot et al., 2022 (Nature Communications), and Waldherr et al., 2024 (Communications Biology). (burkewitz2020atf6regulateslifespan pages 3-5, burkewitz2020atf6regulateslifespan pages 1-3, waldherr2019constitutivexbp1smediatedactivation pages 2-4, beaudoinchabot2022theunfoldedprotein pages 2-3, waldherr2024endoplasmicreticulumunfolded pages 8-9, waldherr2024endoplasmicreticulumunfolded pages 4-5, waldherr2024endoplasmicreticulumunfolded pages 10-11, waldherr2019constitutivexbp1smediatedactivation pages 6-7, waldherr2024endoplasmicreticulumunfolded pages 3-4, waldherr2024endoplasmicreticulumunfolded pages 1-3, waldherr2024endoplasmicreticulumunfolded pages 11-12)

Comprehensive research report: C. elegans atf-6 (UniProt: Q20435)

1) Key concepts and definitions
- Molecular identity and activation: atf-6 encodes an ER-membrane basic leucine zipper (bZIP) transcription factor that functions as one of the three canonical branches of the endoplasmic reticulum unfolded protein response (UPRER) in C. elegans. Under ER stress, ATF-6 dissociates from BiP, traffics to the Golgi, is cleaved to release an N‑terminal transcription factor (ATF-6n), and then translocates to the nucleus to induce ER proteostasis genes; ATF‑6 can cooperate with the IRE‑1/XBP‑1 branch through heterodimerization and co-regulation of ER stress response elements. URL: https://doi.org/10.1038/s41467-019-12070-3 (published Sep 2019); https://doi.org/10.1038/s42003-024-06570-2 (published Jul 2024). (waldherr2019constitutivexbp1smediatedactivation pages 2-4, waldherr2024endoplasmicreticulumunfolded pages 3-4, waldherr2024endoplasmicreticulumunfolded pages 1-3)
- Pathway context: The UPRER has three branches: IRE‑1/xbp‑1, PERK/pek‑1, and ATF‑6/atf‑6. In C. elegans, atf‑6 contributes to ER proteostasis, ER‑mitochondrial signaling, and organismal phenotypes including aging and neuronal proteostasis. URL: https://doi.org/10.1016/j.celrep.2020.108125 (published Sep 2020); https://doi.org/10.1038/s41467-022-33630-0 (published Oct 2022). (burkewitz2020atf6regulateslifespan pages 1-3, beaudoinchabot2022theunfoldedprotein pages 2-3)

2) Function, localization, and mechanisms
- Subcellular localization and mechanism: atf-6 resides in the ER membrane and, upon stress, is transported to the Golgi for regulated intramembrane proteolysis; the cleaved N‑terminal bZIP transcription factor localizes to the nucleus. Cooperative action with XBP‑1s increases transcriptional activation of ER chaperones and ER-associated degradation (ERAD) components. URL: https://doi.org/10.1038/s41467-019-12070-3; https://doi.org/10.1038/s42003-024-06570-2. (waldherr2019constitutivexbp1smediatedactivation pages 2-4, waldherr2024endoplasmicreticulumunfolded pages 3-4, waldherr2024endoplasmicreticulumunfolded pages 1-3)
- Primary functional outputs in C. elegans: Genetic loss of atf-6 reprograms ER calcium handling by downregulating calreticulin/crt‑1, enhances ER-to-mitochondria Ca2+ transfer via the IP3 receptor itr‑1, and improves organismal lifespan and late-life health metrics without overt sensitization to canonical proteotoxic ER stress, indicating a role beyond strict proteostasis. URL: https://doi.org/10.1016/j.celrep.2020.108125. (burkewitz2020atf6regulateslifespan pages 3-5, burkewitz2020atf6regulateslifespan pages 1-3, burkewitz2020atf6regulateslifespan pages 5-6)

3) Quantitative phenotypes and experimental evidence
- Longevity: atf‑6(ok551) deletion increases median lifespan by 57% (p < 0.0001), and an independent CRISPR null increases lifespan by 43% (p < 0.0001), with improved pharyngeal pumping during aging and no major developmental or brood-size defects. Lifespan and healthspan assays were conducted with n ≈ 100/condition and appropriate statistics. URL: https://doi.org/10.1016/j.celrep.2020.108125. (burkewitz2020atf6regulateslifespan pages 3-5)
- Mechanistic genetics: crt‑1(bz29) null phenocopies atf‑6 longevity (~38% lifespan extension vs WT), while reducing itr‑1 function suppresses atf‑6 longevity and an itr‑1(gain-of-function) allele extends lifespan but is not additive with atf‑6, placing ER Ca2+ release via ITPR/itr‑1 downstream of atf‑6. URL: https://doi.org/10.1016/j.celrep.2020.108125. (burkewitz2020atf6regulateslifespan pages 5-6)
- ER–mitochondrial Ca2+ axis: Mitochondrial matrix Ca2+ declines by ~33% from day 1 to day 7 in WT; genetic ablation of the mitochondrial Ca2+ uniporter mcu‑1 reduces atf‑6-dependent lifespan extension by 67%, indicating mitochondrial Ca2+ uptake is necessary for atf‑6 longevity. URL: https://doi.org/10.1016/j.celrep.2020.108125. (burkewitz2020atf6regulateslifespan pages 6-8)
- ER stress/proteostasis readouts: atf‑6 mutants are not hypersensitive to tunicamycin and show relatively modest transcriptomic changes (26 down, 101 up genes) compared to other UPR branches, suggesting atf‑6 longevity is not driven by generalized UPR activation. URL: https://doi.org/10.1016/j.celrep.2020.108125. (burkewitz2020atf6regulateslifespan pages 3-5, burkewitz2020atf6regulateslifespan pages 1-3)

4) Interactions with other UPR branches and neuronal proteostasis
- Requirement for ATF‑6 in XBP‑1s-mediated neuronal rescue: In C. elegans tauopathy models, constitutive neuronal XBP‑1s reduces soluble and phosphorylated tau and rescues locomotor/neuron survival phenotypes, but these protective effects require functional ATF‑6; atf‑6 loss abolishes XBP‑1s-driven rescue, while pek‑1 loss only partially impairs rescue. URL: https://doi.org/10.1038/s41467-019-12070-3 (Sep 2019). (waldherr2019constitutivexbp1smediatedactivation pages 6-7, waldherr2019constitutivexbp1smediatedactivation pages 2-4)
- 2024 updates on downstream targets: RNA‑seq of neuronal XBP‑1s gain‑of‑function defines 116 upregulated targets; five candidates with prior ATF6 association (csp‑1, dnj‑28, hsp‑4/BiP, ckb‑2, lipl‑3) are required individually for XBP‑1s rescue; HSP‑4 overexpression alone partially rescues tauopathy, whereas too-high HSP‑4 can worsen behavior, indicating dose‑dependent effects. Additional required targets include erp‑44.3 (ERP44 ortholog), F41E7.6 (CROT ortholog), C01B4.6 (GALM ortholog), Y19D10A.16, eol‑1, and mct‑2; ERAD (sel‑11/HRD1) is also necessary. URL: https://doi.org/10.1038/s42003-024-06570-2 (Jul 2024). (waldherr2024endoplasmicreticulumunfolded pages 8-9, waldherr2024endoplasmicreticulumunfolded pages 4-5, waldherr2024endoplasmicreticulumunfolded pages 10-11, waldherr2024endoplasmicreticulumunfolded pages 3-4, waldherr2024endoplasmicreticulumunfolded pages 1-3, waldherr2024endoplasmicreticulumunfolded pages 11-12)
- Developmental genetic context: atf‑6 loss shows synthetic interactions with the ire‑1/xbp‑1 pathway during development and acts largely in parallel to pek‑1/IRE‑1 for lifespan effects, highlighting both branch-specific and cooperative roles depending on tissue and context. URL: https://doi.org/10.1016/j.celrep.2020.108125. (burkewitz2020atf6regulateslifespan pages 3-5)

5) Recent developments and 2023–2024 highlights
- Neuronal proteostasis (2024): XBP‑1s rescue of tauopathy requires ATF‑6 and a defined set of downstream effectors, providing a targetable module (HSP‑4/BiP, CKB‑2, LIPL‑3, ERP44 ortholog, and others) for modulating neuronal ER proteostasis. URL: https://doi.org/10.1038/s42003-024-06570-2 (Jul 2024). (waldherr2024endoplasmicreticulumunfolded pages 8-9, waldherr2024endoplasmicreticulumunfolded pages 4-5, waldherr2024endoplasmicreticulumunfolded pages 10-11, waldherr2024endoplasmicreticulumunfolded pages 3-4, waldherr2024endoplasmicreticulumunfolded pages 1-3, waldherr2024endoplasmicreticulumunfolded pages 11-12)
- Metabolic/aging context (2022, proximate to 2023–2024 window): In aged worms (HGD started at day 5), high glucose extends lifespan by activating otherwise quiescent UPRER; ATF‑6 and PEK‑1 contribute to this longevity, while IRE‑1 ablation increases lifespan in young HGD‑1 animals, indicating age‑dependent, branch‑specific effects of the UPRER. URL: https://doi.org/10.1038/s41467-022-33630-0 (Oct 2022). (beaudoinchabot2022theunfoldedprotein pages 2-3)

6) Current applications and real-world implementations
- Aging interventions: Genetic or pharmacologic modulation of the ATF‑6 branch and ER Ca2+ handling (e.g., via calreticulin/crt‑1, itr‑1/IP3R, mcu‑1) is a tractable route to extend lifespan or healthspan in C. elegans, informing conserved ER–mitochondrial signaling axes potentially relevant to aging interventions. URL: https://doi.org/10.1016/j.celrep.2020.108125. (burkewitz2020atf6regulateslifespan pages 3-5, burkewitz2020atf6regulateslifespan pages 6-8, burkewitz2020atf6regulateslifespan pages 5-6)
- Neurodegeneration models: Neuronal activation of UPRER via XBP‑1s with intact ATF‑6 and ERAD machinery mitigates tauopathy phenotypes; defined downstream effectors from 2024 work provide candidate targets for translational exploration of ER proteostasis enhancement. URLs: https://doi.org/10.1038/s41467-019-12070-3; https://doi.org/10.1038/s42003-024-06570-2. (waldherr2019constitutivexbp1smediatedactivation pages 6-7, waldherr2024endoplasmicreticulumunfolded pages 3-4, waldherr2024endoplasmicreticulumunfolded pages 1-3)
- Metabolic reprogramming with age: Controlled UPRER activation under specific age/metabolic conditions (e.g., glucose timing) can reverse age‑related decline, with ATF‑6 among the mediators, guiding experimental designs for late‑life interventions. URL: https://doi.org/10.1038/s41467-022-33630-0. (beaudoinchabot2022theunfoldedprotein pages 2-3)

7) Expert opinions and synthesis
- Cooperative UPRER principle: Multiple lines of evidence indicate that ATF‑6 cooperates with XBP‑1s to mount an adequate ER proteostasis program in neurons and that specific downstream effectors (chaperones like HSP‑4/BiP, ERAD components such as SEL‑11/HRD1, and metabolic enzymes/transporters) are required for proteotoxic stress mitigation. This reinforces a model where ATF‑6 is not merely redundant with IRE‑1/XBP‑1 but is a permissive/co‑regulatory factor in neuronal contexts. URLs: 2019—https://doi.org/10.1038/s41467-019-12070-3; 2024—https://doi.org/10.1038/s42003-024-06570-2. (waldherr2019constitutivexbp1smediatedactivation pages 6-7, waldherr2024endoplasmicreticulumunfolded pages 3-4, waldherr2024endoplasmicreticulumunfolded pages 1-3, waldherr2024endoplasmicreticulumunfolded pages 11-12)
- Calcium-centric aging mechanism: The striking longevity of atf‑6 mutants is best explained by altered ER Ca2+ buffering (via reduced calreticulin), enhanced ER–mitochondrial calcium flux through itr‑1/IP3R and mcu‑1, and downstream remodeling of mitochondrial function/dynamics; this is mechanistically distinct from classical proteostasis induction. URL: https://doi.org/10.1016/j.celrep.2020.108125. (burkewitz2020atf6regulateslifespan pages 3-5, burkewitz2020atf6regulateslifespan pages 6-8, burkewitz2020atf6regulateslifespan pages 5-6)

8) Statistics and key data points
- Lifespan extension: +57% (atf‑6(ok551)); +43% (CRISPR null); crt‑1 null phenocopy ~+38%. URL: https://doi.org/10.1016/j.celrep.2020.108125. (burkewitz2020atf6regulateslifespan pages 3-5, burkewitz2020atf6regulateslifespan pages 5-6)
- Mitochondrial Ca2+ and necessity: WT intestine mito‑Ca2+ declines ~33% with age (day 1→7); mcu‑1 deletion reduces atf‑6 longevity by 67%. URL: https://doi.org/10.1016/j.celrep.2020.108125. (burkewitz2020atf6regulateslifespan pages 6-8)
- Neuronal proteostasis: XBP‑1s rescue requires ATF‑6 and ERAD (sel‑11/HRD1); downstream effectors required include hsp‑4/BiP, dnj‑28, csp‑1, ckb‑2, lipl‑3, erp‑44.3, F41E7.6, C01B4.6, Y19D10A.16, eol‑1, mct‑2; HSP‑4 overexpression alone partially rescues, with dose dependence. URL: https://doi.org/10.1038/s41467-019-12070-3; https://doi.org/10.1038/s42003-024-06570-2. (waldherr2019constitutivexbp1smediatedactivation pages 6-7, waldherr2024endoplasmicreticulumunfolded pages 8-9, waldherr2024endoplasmicreticulumunfolded pages 4-5, waldherr2024endoplasmicreticulumunfolded pages 10-11, waldherr2024endoplasmicreticulumunfolded pages 3-4, waldherr2024endoplasmicreticulumunfolded pages 1-3, waldherr2024endoplasmicreticulumunfolded pages 11-12)
- Metabolic/aging modulation (late-life glucose): HGD started at day 5 extends lifespan with ATF‑6 and PEK‑1 contributions, whereas IRE‑1 ablation increases lifespan when HGD is started at day 1, illustrating branch‑ and age‑specific roles. URL: https://doi.org/10.1038/s41467-022-33630-0. (beaudoinchabot2022theunfoldedprotein pages 2-3)

9) Ambiguity check and domain coherence
- Gene symbol and organism: The literature above consistently refers to atf‑6 in C. elegans and aligns with the UniProt-provided identity (Q20435); domain/family annotations (ATF bZIP) match the reported ER‑membrane transcription factor mechanism and downstream ERSE‑driven gene regulation. No conflicting gene symbol usage from other organisms is cited in the sources summarized here. (waldherr2019constitutivexbp1smediatedactivation pages 2-4, waldherr2024endoplasmicreticulumunfolded pages 3-4)

Open questions and future directions
- Tissue specificity of atf‑6 actions beyond intestine and neurons remains to be defined, including potential roles in glia and muscle. Dissecting direct ATF‑6 chromatin binding targets in C. elegans with CUT&RUN/ChIP‑seq and temporal control could clarify context‑dependent cooperation with XBP‑1s.
- Pharmacological leverage points include calreticulin regulation, ITPR channel modulation, and mitochondrial Ca2+ uptake, but translational relevance requires careful titration given dose‑dependent effects (e.g., HSP‑4/BiP overexpression) observed in neurons. (burkewitz2020atf6regulateslifespan pages 5-6, waldherr2024endoplasmicreticulumunfolded pages 8-9)

References (with URLs and publication dates)
- Burkewitz et al., Cell Reports 2020; “Atf-6 Regulates Lifespan through ER‑Mitochondrial Calcium Homeostasis.” URL: https://doi.org/10.1016/j.celrep.2020.108125 (Sep 2020). (burkewitz2020atf6regulateslifespan pages 3-5, burkewitz2020atf6regulateslifespan pages 6-8, burkewitz2020atf6regulateslifespan pages 1-3, burkewitz2020atf6regulateslifespan pages 10-12, burkewitz2020atf6regulateslifespan pages 5-6, burkewitz2020atf6regulateslifespan pages 12-14)
- Waldherr et al., Nature Communications 2019; “Constitutive XBP‑1s‑mediated activation of the ER UPR protects against pathological tau.” URL: https://doi.org/10.1038/s41467-019-12070-3 (Sep 2019). (waldherr2019constitutivexbp1smediatedactivation pages 2-4, waldherr2019constitutivexbp1smediatedactivation pages 6-7, waldherr2019constitutivexbp1smediatedactivation pages 7-7)
- Beaudoin‑Chabot et al., Nature Communications 2022; “The unfolded protein response reverses the effects of glucose on lifespan in chemically‑sterilized C. elegans.” URL: https://doi.org/10.1038/s41467-022-33630-0 (Oct 2022). (beaudoinchabot2022theunfoldedprotein pages 2-3)
- Waldherr et al., Communications Biology 2024; “Endoplasmic reticulum unfolded protein response transcriptional targets of XBP‑1s mediate rescue from tauopathy.” URL: https://doi.org/10.1038/s42003-024-06570-2 (Jul 2024). (waldherr2024endoplasmicreticulumunfolded pages 8-9, waldherr2024endoplasmicreticulumunfolded pages 4-5, waldherr2024endoplasmicreticulumunfolded pages 10-11, waldherr2024endoplasmicreticulumunfolded pages 3-4, waldherr2024endoplasmicreticulumunfolded pages 1-3, waldherr2024endoplasmicreticulumunfolded pages 11-12)

References

1. (burkewitz2020atf6regulateslifespan pages 3-5): Kristopher Burkewitz, Gaomin Feng, Sneha Dutta, Charlotte A. Kelley, Michael Steinbaugh, Erin J. Cram, and William B. Mair. Atf-6 regulates lifespan through er-mitochondrial calcium homeostasis. Cell Reports, 32:108125, Sep 2020. URL: https://doi.org/10.1016/j.celrep.2020.108125, doi:10.1016/j.celrep.2020.108125. This article has 82 citations and is from a highest quality peer-reviewed journal.

2. (burkewitz2020atf6regulateslifespan pages 1-3): Kristopher Burkewitz, Gaomin Feng, Sneha Dutta, Charlotte A. Kelley, Michael Steinbaugh, Erin J. Cram, and William B. Mair. Atf-6 regulates lifespan through er-mitochondrial calcium homeostasis. Cell Reports, 32:108125, Sep 2020. URL: https://doi.org/10.1016/j.celrep.2020.108125, doi:10.1016/j.celrep.2020.108125. This article has 82 citations and is from a highest quality peer-reviewed journal.

3. (waldherr2019constitutivexbp1smediatedactivation pages 2-4): Sarah M. Waldherr, Timothy J. Strovas, Taylor A. Vadset, Nicole F. Liachko, and Brian C. Kraemer. Constitutive xbp-1s-mediated activation of the endoplasmic reticulum unfolded protein response protects against pathological tau. Nature Communications, Sep 2019. URL: https://doi.org/10.1038/s41467-019-12070-3, doi:10.1038/s41467-019-12070-3. This article has 66 citations and is from a highest quality peer-reviewed journal.

4. (beaudoinchabot2022theunfoldedprotein pages 2-3): Caroline Beaudoin-Chabot, Lei Wang, Cenk Celik, Aishah Tul-Firdaus Abdul Khalid, Subhash Thalappilly, Shiyi Xu, Jhee Hong Koh, Venus Wen Xuan Lim, Ann Don Low, and Guillaume Thibault. The unfolded protein response reverses the effects of glucose on lifespan in chemically-sterilized c. elegans. Nature Communications, Oct 2022. URL: https://doi.org/10.1038/s41467-022-33630-0, doi:10.1038/s41467-022-33630-0. This article has 27 citations and is from a highest quality peer-reviewed journal.

5. (waldherr2024endoplasmicreticulumunfolded pages 8-9): Sarah M. Waldherr, Marina Han, Aleen D. Saxton, Taylor A. Vadset, Pamela J. McMillan, Jeanna M. Wheeler, Nicole F. Liachko, and Brian C. Kraemer. Endoplasmic reticulum unfolded protein response transcriptional targets of xbp-1s mediate rescue from tauopathy. Communications Biology, Jul 2024. URL: https://doi.org/10.1038/s42003-024-06570-2, doi:10.1038/s42003-024-06570-2. This article has 3 citations and is from a peer-reviewed journal.

6. (waldherr2024endoplasmicreticulumunfolded pages 4-5): Sarah M. Waldherr, Marina Han, Aleen D. Saxton, Taylor A. Vadset, Pamela J. McMillan, Jeanna M. Wheeler, Nicole F. Liachko, and Brian C. Kraemer. Endoplasmic reticulum unfolded protein response transcriptional targets of xbp-1s mediate rescue from tauopathy. Communications Biology, Jul 2024. URL: https://doi.org/10.1038/s42003-024-06570-2, doi:10.1038/s42003-024-06570-2. This article has 3 citations and is from a peer-reviewed journal.

7. (waldherr2024endoplasmicreticulumunfolded pages 10-11): Sarah M. Waldherr, Marina Han, Aleen D. Saxton, Taylor A. Vadset, Pamela J. McMillan, Jeanna M. Wheeler, Nicole F. Liachko, and Brian C. Kraemer. Endoplasmic reticulum unfolded protein response transcriptional targets of xbp-1s mediate rescue from tauopathy. Communications Biology, Jul 2024. URL: https://doi.org/10.1038/s42003-024-06570-2, doi:10.1038/s42003-024-06570-2. This article has 3 citations and is from a peer-reviewed journal.

8. (waldherr2019constitutivexbp1smediatedactivation pages 6-7): Sarah M. Waldherr, Timothy J. Strovas, Taylor A. Vadset, Nicole F. Liachko, and Brian C. Kraemer. Constitutive xbp-1s-mediated activation of the endoplasmic reticulum unfolded protein response protects against pathological tau. Nature Communications, Sep 2019. URL: https://doi.org/10.1038/s41467-019-12070-3, doi:10.1038/s41467-019-12070-3. This article has 66 citations and is from a highest quality peer-reviewed journal.

9. (waldherr2024endoplasmicreticulumunfolded pages 3-4): Sarah M. Waldherr, Marina Han, Aleen D. Saxton, Taylor A. Vadset, Pamela J. McMillan, Jeanna M. Wheeler, Nicole F. Liachko, and Brian C. Kraemer. Endoplasmic reticulum unfolded protein response transcriptional targets of xbp-1s mediate rescue from tauopathy. Communications Biology, Jul 2024. URL: https://doi.org/10.1038/s42003-024-06570-2, doi:10.1038/s42003-024-06570-2. This article has 3 citations and is from a peer-reviewed journal.

10. (waldherr2024endoplasmicreticulumunfolded pages 1-3): Sarah M. Waldherr, Marina Han, Aleen D. Saxton, Taylor A. Vadset, Pamela J. McMillan, Jeanna M. Wheeler, Nicole F. Liachko, and Brian C. Kraemer. Endoplasmic reticulum unfolded protein response transcriptional targets of xbp-1s mediate rescue from tauopathy. Communications Biology, Jul 2024. URL: https://doi.org/10.1038/s42003-024-06570-2, doi:10.1038/s42003-024-06570-2. This article has 3 citations and is from a peer-reviewed journal.

11. (waldherr2024endoplasmicreticulumunfolded pages 11-12): Sarah M. Waldherr, Marina Han, Aleen D. Saxton, Taylor A. Vadset, Pamela J. McMillan, Jeanna M. Wheeler, Nicole F. Liachko, and Brian C. Kraemer. Endoplasmic reticulum unfolded protein response transcriptional targets of xbp-1s mediate rescue from tauopathy. Communications Biology, Jul 2024. URL: https://doi.org/10.1038/s42003-024-06570-2, doi:10.1038/s42003-024-06570-2. This article has 3 citations and is from a peer-reviewed journal.

12. (burkewitz2020atf6regulateslifespan pages 5-6): Kristopher Burkewitz, Gaomin Feng, Sneha Dutta, Charlotte A. Kelley, Michael Steinbaugh, Erin J. Cram, and William B. Mair. Atf-6 regulates lifespan through er-mitochondrial calcium homeostasis. Cell Reports, 32:108125, Sep 2020. URL: https://doi.org/10.1016/j.celrep.2020.108125, doi:10.1016/j.celrep.2020.108125. This article has 82 citations and is from a highest quality peer-reviewed journal.

13. (burkewitz2020atf6regulateslifespan pages 6-8): Kristopher Burkewitz, Gaomin Feng, Sneha Dutta, Charlotte A. Kelley, Michael Steinbaugh, Erin J. Cram, and William B. Mair. Atf-6 regulates lifespan through er-mitochondrial calcium homeostasis. Cell Reports, 32:108125, Sep 2020. URL: https://doi.org/10.1016/j.celrep.2020.108125, doi:10.1016/j.celrep.2020.108125. This article has 82 citations and is from a highest quality peer-reviewed journal.

14. (burkewitz2020atf6regulateslifespan pages 10-12): Kristopher Burkewitz, Gaomin Feng, Sneha Dutta, Charlotte A. Kelley, Michael Steinbaugh, Erin J. Cram, and William B. Mair. Atf-6 regulates lifespan through er-mitochondrial calcium homeostasis. Cell Reports, 32:108125, Sep 2020. URL: https://doi.org/10.1016/j.celrep.2020.108125, doi:10.1016/j.celrep.2020.108125. This article has 82 citations and is from a highest quality peer-reviewed journal.

15. (burkewitz2020atf6regulateslifespan pages 12-14): Kristopher Burkewitz, Gaomin Feng, Sneha Dutta, Charlotte A. Kelley, Michael Steinbaugh, Erin J. Cram, and William B. Mair. Atf-6 regulates lifespan through er-mitochondrial calcium homeostasis. Cell Reports, 32:108125, Sep 2020. URL: https://doi.org/10.1016/j.celrep.2020.108125, doi:10.1016/j.celrep.2020.108125. This article has 82 citations and is from a highest quality peer-reviewed journal.

16. (waldherr2019constitutivexbp1smediatedactivation pages 7-7): Sarah M. Waldherr, Timothy J. Strovas, Taylor A. Vadset, Nicole F. Liachko, and Brian C. Kraemer. Constitutive xbp-1s-mediated activation of the endoplasmic reticulum unfolded protein response protects against pathological tau. Nature Communications, Sep 2019. URL: https://doi.org/10.1038/s41467-019-12070-3, doi:10.1038/s41467-019-12070-3. This article has 66 citations and is from a highest quality peer-reviewed journal.

Citations

1. beaudoinchabot2022theunfoldedprotein pages 2-3
2. waldherr2024endoplasmicreticulumunfolded pages 8-9
3. waldherr2024endoplasmicreticulumunfolded pages 4-5
4. waldherr2024endoplasmicreticulumunfolded pages 10-11
5. waldherr2024endoplasmicreticulumunfolded pages 3-4
6. waldherr2024endoplasmicreticulumunfolded pages 1-3
7. waldherr2024endoplasmicreticulumunfolded pages 11-12
8. https://doi.org/10.1038/s41467-019-12070-3
9. https://doi.org/10.1038/s42003-024-06570-2
10. https://doi.org/10.1016/j.celrep.2020.108125
11. https://doi.org/10.1038/s41467-022-33630-0
12. https://doi.org/10.1038/s41467-019-12070-3;
13. https://doi.org/10.1038/s42003-024-06570-2.
14. https://doi.org/10.1016/j.celrep.2020.108125.
15. https://doi.org/10.1038/s41467-022-33630-0.
16. https://doi.org/10.1016/j.celrep.2020.108125,
17. https://doi.org/10.1038/s41467-019-12070-3,
18. https://doi.org/10.1038/s41467-022-33630-0,
19. https://doi.org/10.1038/s42003-024-06570-2,