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this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.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.
ANKZF1 (also published as ZNF744) is the human ortholog of yeast Vms1, and the retrieved literature consistently uses this identity in the context of ribosome-associated quality control (RQC), p97/VCP cofactor biology, and stress-responsive mitochondrial quality control (stapf2011thegeneraldefinition pages 2-3, stapf2011thegeneraldefinition pages 1-1, haaftenvisser2017ankyrinrepeatand pages 1-2). ANKZF1 is therefore the correct human target corresponding to the UniProt accession Q9H8Y5 provided by the user.
A key identity-defining feature is the presence of a VCP/p97-interacting motif (VIM) within ANKZF1/ZNF744, which binds the N-terminal domain of p97/VCP; this motif family was formalized by a minimal consensus RX5AAX2R, and ANKZF1/ZNF744 is explicitly included among VIM-containing p97 cofactors (stapf2011thegeneraldefinition pages 2-3, stapf2011thegeneraldefinition pages 1-1).
RQC is a conserved surveillance system that resolves stalled translation and targets incomplete nascent polypeptides for clearance. In mammals, stalled/collided ribosomes are recognized by the E3 ligase ZNF598, which ubiquitinates 40S proteins and promotes downstream splitting into a peptidyl‑tRNA–bound 60S complex that becomes a substrate for RQC processing (inada2020qualitycontrolsinduced pages 5-5, miscicka2024ribosomalcollisionis pages 1-2).
Across primary and review literature, ANKZF1 is positioned as the factor that liberates nascent chains from 60S peptidyl‑tRNA complexes during RQC, enabling subsequent p97/VCP-driven extraction and proteasomal degradation of aberrant translation products (inada2020qualitycontrolsinduced pages 5-5, inada2020qualitycontrolsinduced pages 5-6).
A mechanistic point of emphasis is that ANKZF1 is best-supported as a tRNA-cleaving endonuclease-like activity acting on the acceptor arm/CCA end of P-site peptidyl‑tRNAs on 60S RQC complexes, rather than a canonical eRF1-like peptidyl‑tRNA hydrolase in mammals (kuroha2018releaseofubiquitinated pages 2-4, yip2020elac1repairstrnas pages 1-3). This difference has led to mixed terminology (“peptidyl‑tRNA hydrolase” in some reviews vs “tRNA endonuclease/acceptor-arm cleavage” in reconstitution studies), but both descriptions converge on the same functional outcome: release of the nascent chain from the tRNA/60S complex as a prerequisite for clearance (kuroha2018releaseofubiquitinated pages 2-4, inada2020qualitycontrolsinduced pages 5-6, inada2020qualitycontrolsinduced pages 5-5).
The experimentally supported substrate is the peptidyl‑tRNA resident on stalled 60S ribosome–nascent chain complexes that arise after stalled ribosomes are split and RQC factors assemble (yip2020elac1repairstrnas pages 1-3, inada2020qualitycontrolsinduced pages 5-6).
Evidence supports that ANKZF1 cleaves the tRNA 3′ end / acceptor-arm region, removing the universally conserved CCA (positions 74–76) and generating a tRNA product that carries a 2′,3′-cyclic phosphate at the discriminator base N73 (yip2020elac1repairstrnas pages 1-3, inada2020qualitycontrolsinduced pages 5-6).
A quantitative detail from in vitro mammalian reconstitution is that the released ubiquitinated nascent chain can remain linked to a short 3′ terminal tRNA remnant; one reported value is four 3′-terminal tRNA nucleotides remaining attached to released ubiquitinated nascent chains (Ub‑NCs) (kuroha2018releaseofubiquitinated pages 1-2). Other mechanistic frameworks/reviews reiterate release of Ub‑NCs linked to three 3′ terminal nucleotides (miscicka2024ribosomalcollisionis pages 1-2), highlighting that the exact remnant length can be described slightly differently depending on experimental context and citation lineage.
Because ANKZF1 cleavage generates a noncanonical tRNA end (including a cyclic phosphate), the tRNA must be repaired before reuse. In mammals, ELAC1 is supported as the repair enzyme: purified ELAC1 can process the cyclic-phosphate-ended tRNA species into a form that becomes a substrate for the CCA-adding enzyme TRNT1, enabling tRNA recycling (yip2020elac1repairstrnas pages 4-6).
A current mammalian pathway model consistent with the retrieved evidence is:
A visual summary of this mechanism (contrasting ANKZF1-mediated processing with Ptrh1-mediated release of non-ubiquitinated substrates) is shown in the graphical abstract of Kuroha et al. 2018 (kuroha2018releaseofubiquitinated media cd140b48).
ANKZF1 contains a VIM that mediates interaction with p97/VCP. The motif consensus RX5AAX2R was defined as a minimal p97-binding element, and experimental approaches including pull-downs, yeast two-hybrid, and NMR mapping support VIM-mediated binding to the p97 N-domain (stapf2011thegeneraldefinition pages 2-3, stapf2011thegeneraldefinition pages 3-4). This interaction is central to positioning ANKZF1 within p97-linked proteostasis networks.
ANKZF1 function is coupled with core RQC factors including NEMF, Listerin/LTN1, and the p97/VCP extraction module, with ANKZF1 acting after 60S RQC complex formation to enable downstream degradation (yip2020elac1repairstrnas pages 1-3, inada2020qualitycontrolsinduced pages 5-5).
Baseline localization: In human cells, ANKZF1 is reported as diffuse/cytosolic under basal conditions (haaftenvisser2017ankyrinrepeatand pages 1-2).
Stress-induced relocalization: Under cellular stress (notably oxidative stress), ANKZF1 translocates to mitochondria, and this can occur together with VCP (haaftenvisser2017ankyrinrepeatand pages 3-4, haaftenvisser2017ankyrinrepeatand pages 1-2). Functionally, ANKZF1 depletion reduces mitochondrial integrity and respiration under stress conditions, linking its localization dynamics to mitochondrial homeostasis (haaftenvisser2017ankyrinrepeatand pages 2-3, haaftenvisser2017ankyrinrepeatand pages 1-2).
A 2024 Nucleic Acids Research study found that depletion of ANKZF1 (alongside other RQC factors) increases accumulation of repeat-associated non-AUG (RAN) translation products from G4C2 (C9ORF72) and CGG (FMR1) repeats, while overexpression of ANKZF1 reduces RAN products in reporters and decreases GP dipeptide repeat abundance in C9 patient iPSC-derived neurons (tseng2024ribosomalqualitycontrol pages 16-18). The same study reports that loss of ANKZF1 had the greatest impact among tested modifiers on RAN product accumulation, supporting ANKZF1 as a potent limiter of toxic repeat translation outputs (tseng2024ribosomalqualitycontrol pages 18-20).
A 2024 Nature Communications paper (focused on ZNF598 regulation) explicitly situates ANKZF1 within mitochondrial-stress-responsive RQC steps: stalled translation triggers downstream quality control events including release of stalled nascent chains from the peptidyl‑tRNA/60S complex by ANKZF1 (geng2024stalledtranslationby pages 1-2).
A 2024 Protein & Cell study using genome-edited human ESC-derived vascular lineages reports that ANKZF1 acts as a novel HIF‑1α target gene in human mesenchymal stem cells (hMSCs). ANKZF1 knockout hMSCs displayed reduced migration and tube formation under hypoxia, consistent with ANKZF1 contributing to pro-angiogenic processes (lei2024humanescderivedvascular pages 10-11).
Biallelic ANKZF1 mutations were associated with infantile-onset inflammatory bowel disease, and patient-derived cellular phenotypes included increased apoptosis and reduced mitochondrial respiration; mechanistically, wild-type ANKZF1 is cytosolic but translocates to mitochondria upon stress, whereas at least one patient allele (R585Q) showed impaired stress-induced translocation (haaftenvisser2017ankyrinrepeatand pages 1-2, haaftenvisser2017ankyrinrepeatand pages 3-4). This represents a direct human disease link and provides a functional assay framework (stress-induced mitochondrial recruitment/respiration) for variant interpretation.
A TCGA-based survival analysis reported that high ANKZF1 expression is associated with poorer outcomes in colon cancer: overall survival HR 2.094 (95% CI 1.188–3.689; p=0.011) and recurrence-free survival HR 1.762 (95% CI 1.021–3.042; p=0.042) (zhou2019highankzf1expression pages 1-2). Additional models reported significant associations for CRC overall (e.g., OS HR 1.661, p=0.007; RFS HR 1.969, p=0.001) and colon-specific analyses (zhou2019highankzf1expression pages 2-4). These results motivate ANKZF1 as a candidate prognostic biomarker and as a gene to integrate into angiogenesis/proteostasis pathway models.
The 2024 repeat-expansion work proposes that augmenting RQC (including ANKZF1 activity) might reduce toxic repeat-derived products, suggesting a translational hypothesis relevant to currently untreatable repeat expansion disorders (tseng2024ribosomalqualitycontrol pages 1-5, tseng2024ribosomalqualitycontrol pages 16-18). This is still preclinical (cellular/iPSC-derived neuron systems), but it defines a clear experimental intervention: overexpression or enhancement of RQC factors.
Open Targets reports ANKZF1 associations with inflammatory bowel disease, neurodegenerative disease, lysosomal storage disease, Alzheimer disease, and Parkinson disease, with scores (e.g., neurodegenerative disease score ~0.555) driven largely by pathway-perturbation signals in CRISPRi screens in neuronal contexts (OpenTargets Search: -ANKZF1). This supports prioritization of ANKZF1 in functional genomics pipelines, although it should be interpreted as associative/screen-derived rather than causal clinical proof.
Mechanistic reviews place ANKZF1/Vms1 as the factor responsible for releasing nascent chains from peptidyl‑tRNA on 60S RQC complexes, upstream of p97/VCP extraction and proteasomal degradation, and emphasize that RQC intersects with organelle-localized translation/proteostasis (inada2020qualitycontrolsinduced pages 5-6, inada2020qualitycontrolsinduced pages 5-5). A key expert-level nuance is that mammalian biochemical reconstitution supports a cleavage mechanism in the tRNA acceptor arm/CCA end rather than a canonical GGQ-like hydrolysis mechanism, explaining persistent terminology differences while preserving agreement on functional role (kuroha2018releaseofubiquitinated pages 2-4, yip2020elac1repairstrnas pages 1-3).
| Category | Evidence summary | Key citations | Publication date & URL |
|---|---|---|---|
| Identity/domains | Human ANKZF1 corresponds to UniProt Q9H8Y5 and the literature synonym ZNF744; it is the mammalian ortholog of yeast Vms1 and contains ankyrin repeats, zinc-finger regions, a mitochondrial targeting domain (MTD), and a VCP/p97-interacting motif (VIM). The VIM consensus was defined as RX5AAX2R and is necessary/sufficient for p97 binding. | (stapf2011thegeneraldefinition pages 2-3, stapf2011thegeneraldefinition pages 1-1, kuroha2018releaseofubiquitinated pages 2-4) | 2011-11-04, https://doi.org/10.1074/jbc.m111.274472; 2018-10-11, https://doi.org/10.1016/j.molcel.2018.08.022 |
| Enzymatic activity | ANKZF1 is experimentally supported as an RQC-associated tRNA-cleaving factor that releases stalled nascent chains from 60S complexes. In mammalian systems it cleaves the acceptor arm/CCA end of peptidyl-tRNA, although some reviews describe the overall outcome as peptidyl-tRNA hydrolysis; the mechanistic consensus is release of nascent chains by ANKZF1 at stalled 60S ribosomes. | (kuroha2018releaseofubiquitinated pages 2-4, yip2020elac1repairstrnas pages 1-3, inada2020qualitycontrolsinduced pages 5-6, inada2020qualitycontrolsinduced pages 5-5) | 2018-10-11, https://doi.org/10.1016/j.molcel.2018.08.022; 2020-02-18, https://doi.org/10.1016/j.celrep.2020.01.082; 2020-01-27, https://doi.org/10.1093/nar/gkz1201 |
| Substrate & products | The substrate is peptidyl-tRNA on stalled 60S ribosome–nascent chain complexes in RQC. ANKZF1 removes CCA74-76, generating a tRNA with a 2',3'-cyclic phosphate at discriminator base N73, and released nascent chains remain attached to a short tRNA remnant reported as 3-4 terminal nucleotides depending on assay/context. | (yip2020elac1repairstrnas pages 1-3, kuroha2018releaseofubiquitinated pages 1-2, miscicka2024ribosomalcollisionis pages 1-2) | 2020-02-18, https://doi.org/10.1016/j.celrep.2020.01.082; 2018-10-11, https://doi.org/10.1016/j.molcel.2018.08.022; 2024-02-29, https://doi.org/10.1093/nar/gkae087 |
| Pathway context (RQC steps) | In canonical mammalian RQC, ribosome stalling/collision triggers ZNF598-mediated 40S ubiquitination and ASCC-dependent splitting; NEMF and Listerin act on the 60S nascent-chain complex, and ANKZF1 then releases the stalled nascent chain for downstream p97/VCP extraction and proteasomal degradation. Cleaved tRNAs are repaired by ELAC1 and then re-CCA-added by TRNT1. | (inada2020qualitycontrolsinduced pages 5-5, inada2020qualitycontrolsinduced pages 5-6, yip2020elac1repairstrnas pages 4-6, miscicka2024ribosomalcollisionis pages 1-2) | 2020-01-27, https://doi.org/10.1093/nar/gkz1201; 2020-02-18, https://doi.org/10.1016/j.celrep.2020.01.082; 2024-02-29, https://doi.org/10.1093/nar/gkae087 |
| Key interactors | Key pathway partners include VCP/p97 (via the VIM), NEMF/Rqc2, Listerin/LTN1, UFD1/NPLOC4, ELAC1, and TRNT1. Evidence supports direct VIM-dependent p97 binding through the p97 N-domain and functional coupling of ANKZF1 to ubiquitinated 60S RQC substrates. | (stapf2011thegeneraldefinition pages 2-3, stapf2011thegeneraldefinition pages 3-4, yip2020elac1repairstrnas pages 1-3, inada2020qualitycontrolsinduced pages 5-5) | 2011-11-04, https://doi.org/10.1074/jbc.m111.274472; 2020-02-18, https://doi.org/10.1016/j.celrep.2020.01.082; 2020-01-27, https://doi.org/10.1093/nar/gkz1201 |
| Subcellular localization | Basally, human ANKZF1 is predominantly diffuse/cytosolic, but upon cellular or mitochondrial stress it relocalizes to mitochondria, often together with VCP. Loss-of-function alleles can impair this stress-induced mitochondrial translocation and are associated with reduced mitochondrial integrity/respiration. | (haaftenvisser2017ankyrinrepeatand pages 1-2, haaftenvisser2017ankyrinrepeatand pages 3-4, haaftenvisser2017ankyrinrepeatand pages 2-3) | 2017-05-12, https://doi.org/10.1074/jbc.m116.772038 |
| Recent 2023-2024 developments | In 2024, ANKZF1 was identified as a strong suppressor of toxic RAN translation from GC-rich repeats in reporter systems and C9ALS/FTD patient iPSC-derived neurons; loss of ANKZF1 had among the largest effects on RAN product accumulation. Other 2024 work placed ANKZF1 within mitochondrial-stress-responsive RQC and identified it as a HIF-1α target contributing to angiogenic phenotypes in human MSCs. | (tseng2024ribosomalqualitycontrol pages 18-20, tseng2024ribosomalqualitycontrol pages 16-18, geng2024stalledtranslationby pages 1-2, lei2024humanescderivedvascular pages 1-2, lei2024humanescderivedvascular pages 10-11) | 2024-02-29, https://doi.org/10.1093/nar/gkae137; 2024-02-22, https://doi.org/10.1038/s41467-024-45525-3; 2024-05-08, https://doi.org/10.1093/procel/pwad027 |
| Disease/translational relevance | Biallelic ANKZF1 mutations are associated with infantile-onset inflammatory bowel disease with apoptosis and mitochondrial respiration defects in patient cells. High ANKZF1 expression is also associated with worse colon cancer outcomes, and platform-level evidence links ANKZF1 to neurodegenerative, lysosomal, Alzheimer, and Parkinson disease contexts. | (haaftenvisser2017ankyrinrepeatand pages 1-2, zhou2019highankzf1expression pages 1-2, OpenTargets Search: -ANKZF1, tseng2024ribosomalqualitycontrol pages 16-18) | 2017-05-12, https://doi.org/10.1074/jbc.m116.772038; 2019-06, https://doi.org/10.2217/fon-2018-0920; 2025, Open Targets Platform reference in Nucleic Acids Research |
| Key quantitative stats | Colon cancer studies reported high ANKZF1 expression associated with poorer overall survival and recurrence-free survival: HR 2.094 (95% CI 1.188-3.689; p=0.011) and HR 1.762 (95% CI 1.021-3.042; p=0.042); broader CRC analyses also reported OS HR 1.661 (95% CI 1.145-2.408; p=0.007) and RFS HR 1.969 (95% CI 1.299-2.984; p=0.001). Open Targets disease association scores included neurodegenerative disease 0.555, lysosomal storage disease 0.428, inflammatory bowel disease 0.374, Alzheimer disease 0.240, and Parkinson disease 0.233. | (zhou2019highankzf1expression pages 8-9, zhou2019highankzf1expression pages 2-4, OpenTargets Search: -ANKZF1) | 2019-06, https://doi.org/10.2217/fon-2018-0920; 2025, Open Targets Platform reference in Nucleic Acids Research |
Table: This table summarizes experimentally supported functions, pathway context, localization, interactors, and translational relevance for human ANKZF1/Q9H8Y5. It is designed as a compact evidence map for downstream functional annotation and report writing.
References
(stapf2011thegeneraldefinition pages 2-3): Christopher Stapf, Edward Cartwright, Mark Bycroft, Kay Hofmann, and Alexander Buchberger. The general definition of the p97/valosin-containing protein (vcp)-interacting motif (vim) delineates a new family of p97 cofactors. Journal of Biological Chemistry, 286:38670-38678, Nov 2011. URL: https://doi.org/10.1074/jbc.m111.274472, doi:10.1074/jbc.m111.274472. This article has 81 citations and is from a domain leading peer-reviewed journal.
(stapf2011thegeneraldefinition pages 1-1): Christopher Stapf, Edward Cartwright, Mark Bycroft, Kay Hofmann, and Alexander Buchberger. The general definition of the p97/valosin-containing protein (vcp)-interacting motif (vim) delineates a new family of p97 cofactors. Journal of Biological Chemistry, 286:38670-38678, Nov 2011. URL: https://doi.org/10.1074/jbc.m111.274472, doi:10.1074/jbc.m111.274472. This article has 81 citations and is from a domain leading peer-reviewed journal.
(haaftenvisser2017ankyrinrepeatand pages 1-2): Désirée Y. van Haaften-Visser, Magdalena Harakalova, Enric Mocholi, Joris M. van Montfrans, Abdul Elkadri, Ester Rieter, Karoline Fiedler, Peter M. van Hasselt, Emily M.M. Triffaux, Mieke M. van Haelst, Isaac J. Nijman, Wigard P. Kloosterman, Edward E.S. Nieuwenhuis, Aleixo M. Muise, Edwin Cuppen, Roderick H.J. Houwen, and Paul J. Coffer. Ankyrin repeat and zinc-finger domain-containing 1 mutations are associated with infantile-onset inflammatory bowel disease. Journal of Biological Chemistry, 292:7904-7920, May 2017. URL: https://doi.org/10.1074/jbc.m116.772038, doi:10.1074/jbc.m116.772038. This article has 39 citations and is from a domain leading peer-reviewed journal.
(inada2020qualitycontrolsinduced pages 5-5): Toshifumi Inada. Quality controls induced by aberrant translation. Nucleic Acids Research, 48:1084-1096, Jan 2020. URL: https://doi.org/10.1093/nar/gkz1201, doi:10.1093/nar/gkz1201. This article has 136 citations and is from a highest quality peer-reviewed journal.
(miscicka2024ribosomalcollisionis pages 1-2): Anna Miścicka, Alexander G Bulakhov, Kazushige Kuroha, Alexandra Zinoviev, Christopher U T Hellen, and Tatyana V Pestova. Ribosomal collision is not a prerequisite for znf598-mediated ribosome ubiquitination and disassembly of ribosomal complexes by ascc. Nucleic Acids Research, 52:4627-4643, Feb 2024. URL: https://doi.org/10.1093/nar/gkae087, doi:10.1093/nar/gkae087. This article has 21 citations and is from a highest quality peer-reviewed journal.
(inada2020qualitycontrolsinduced pages 5-6): Toshifumi Inada. Quality controls induced by aberrant translation. Nucleic Acids Research, 48:1084-1096, Jan 2020. URL: https://doi.org/10.1093/nar/gkz1201, doi:10.1093/nar/gkz1201. This article has 136 citations and is from a highest quality peer-reviewed journal.
(kuroha2018releaseofubiquitinated pages 2-4): Kazushige Kuroha, Alexandra Zinoviev, Christopher U.T. Hellen, and Tatyana V. Pestova. Release of ubiquitinated and non-ubiquitinated nascent chains from stalled mammalian ribosomal complexes by ankzf1 and ptrh1. Molecular cell, 72 2:286-302.e8, Oct 2018. URL: https://doi.org/10.1016/j.molcel.2018.08.022, doi:10.1016/j.molcel.2018.08.022. This article has 127 citations and is from a highest quality peer-reviewed journal.
(yip2020elac1repairstrnas pages 1-3): Matthew C.J. Yip, Simonas Savickas, Steven P. Gygi, and Sichen Shao. Elac1 repairs trnas cleaved during ribosome-associated quality control. Cell reports, 30 7:2106-2114.e5, Feb 2020. URL: https://doi.org/10.1016/j.celrep.2020.01.082, doi:10.1016/j.celrep.2020.01.082. This article has 47 citations and is from a highest quality peer-reviewed journal.
(kuroha2018releaseofubiquitinated pages 1-2): Kazushige Kuroha, Alexandra Zinoviev, Christopher U.T. Hellen, and Tatyana V. Pestova. Release of ubiquitinated and non-ubiquitinated nascent chains from stalled mammalian ribosomal complexes by ankzf1 and ptrh1. Molecular cell, 72 2:286-302.e8, Oct 2018. URL: https://doi.org/10.1016/j.molcel.2018.08.022, doi:10.1016/j.molcel.2018.08.022. This article has 127 citations and is from a highest quality peer-reviewed journal.
(yip2020elac1repairstrnas pages 4-6): Matthew C.J. Yip, Simonas Savickas, Steven P. Gygi, and Sichen Shao. Elac1 repairs trnas cleaved during ribosome-associated quality control. Cell reports, 30 7:2106-2114.e5, Feb 2020. URL: https://doi.org/10.1016/j.celrep.2020.01.082, doi:10.1016/j.celrep.2020.01.082. This article has 47 citations and is from a highest quality peer-reviewed journal.
(mcgirr2025dysregulatedribosomequality pages 2-4): Tom McGirr, Okan Onar, and Seyed Mehdi Jafarnejad. Dysregulated ribosome quality control in human diseases. The Febs Journal, 292:936-959, Jul 2025. URL: https://doi.org/10.1111/febs.17217, doi:10.1111/febs.17217. This article has 20 citations.
(kuroha2018releaseofubiquitinated media cd140b48): Kazushige Kuroha, Alexandra Zinoviev, Christopher U.T. Hellen, and Tatyana V. Pestova. Release of ubiquitinated and non-ubiquitinated nascent chains from stalled mammalian ribosomal complexes by ankzf1 and ptrh1. Molecular cell, 72 2:286-302.e8, Oct 2018. URL: https://doi.org/10.1016/j.molcel.2018.08.022, doi:10.1016/j.molcel.2018.08.022. This article has 127 citations and is from a highest quality peer-reviewed journal.
(stapf2011thegeneraldefinition pages 3-4): Christopher Stapf, Edward Cartwright, Mark Bycroft, Kay Hofmann, and Alexander Buchberger. The general definition of the p97/valosin-containing protein (vcp)-interacting motif (vim) delineates a new family of p97 cofactors. Journal of Biological Chemistry, 286:38670-38678, Nov 2011. URL: https://doi.org/10.1074/jbc.m111.274472, doi:10.1074/jbc.m111.274472. This article has 81 citations and is from a domain leading peer-reviewed journal.
(haaftenvisser2017ankyrinrepeatand pages 3-4): Désirée Y. van Haaften-Visser, Magdalena Harakalova, Enric Mocholi, Joris M. van Montfrans, Abdul Elkadri, Ester Rieter, Karoline Fiedler, Peter M. van Hasselt, Emily M.M. Triffaux, Mieke M. van Haelst, Isaac J. Nijman, Wigard P. Kloosterman, Edward E.S. Nieuwenhuis, Aleixo M. Muise, Edwin Cuppen, Roderick H.J. Houwen, and Paul J. Coffer. Ankyrin repeat and zinc-finger domain-containing 1 mutations are associated with infantile-onset inflammatory bowel disease. Journal of Biological Chemistry, 292:7904-7920, May 2017. URL: https://doi.org/10.1074/jbc.m116.772038, doi:10.1074/jbc.m116.772038. This article has 39 citations and is from a domain leading peer-reviewed journal.
(haaftenvisser2017ankyrinrepeatand pages 2-3): Désirée Y. van Haaften-Visser, Magdalena Harakalova, Enric Mocholi, Joris M. van Montfrans, Abdul Elkadri, Ester Rieter, Karoline Fiedler, Peter M. van Hasselt, Emily M.M. Triffaux, Mieke M. van Haelst, Isaac J. Nijman, Wigard P. Kloosterman, Edward E.S. Nieuwenhuis, Aleixo M. Muise, Edwin Cuppen, Roderick H.J. Houwen, and Paul J. Coffer. Ankyrin repeat and zinc-finger domain-containing 1 mutations are associated with infantile-onset inflammatory bowel disease. Journal of Biological Chemistry, 292:7904-7920, May 2017. URL: https://doi.org/10.1074/jbc.m116.772038, doi:10.1074/jbc.m116.772038. This article has 39 citations and is from a domain leading peer-reviewed journal.
(tseng2024ribosomalqualitycontrol pages 16-18): Yi-Ju Tseng, Amy Krans, Indranil Malik, Xiexiong Deng, Evrim Yildirim, Sinem Ovunc, Elizabeth M H Tank, Karen Jansen-West, Ross Kaufhold, Nicolas B Gomez, Roger Sher, Leonard Petrucelli, Sami J Barmada, and Peter K Todd. Ribosomal quality control factors inhibit repeat-associated non-aug translation from gc-rich repeats. Nucleic Acids Research, 52:5928-5949, Feb 2024. URL: https://doi.org/10.1093/nar/gkae137, doi:10.1093/nar/gkae137. This article has 21 citations and is from a highest quality peer-reviewed journal.
(tseng2024ribosomalqualitycontrol pages 18-20): Yi-Ju Tseng, Amy Krans, Indranil Malik, Xiexiong Deng, Evrim Yildirim, Sinem Ovunc, Elizabeth M H Tank, Karen Jansen-West, Ross Kaufhold, Nicolas B Gomez, Roger Sher, Leonard Petrucelli, Sami J Barmada, and Peter K Todd. Ribosomal quality control factors inhibit repeat-associated non-aug translation from gc-rich repeats. Nucleic Acids Research, 52:5928-5949, Feb 2024. URL: https://doi.org/10.1093/nar/gkae137, doi:10.1093/nar/gkae137. This article has 21 citations and is from a highest quality peer-reviewed journal.
(geng2024stalledtranslationby pages 1-2): Ji Geng, Shuangxi Li, Yu Li, Zhihao Wu, Sunil Bhurtel, Suman Rimal, Danish Khan, Rani Ohja, Onn Brandman, and Bingwei Lu. Stalled translation by mitochondrial stress upregulates a cnot4-znf598 ribosomal quality control pathway important for tissue homeostasis. Nature Communications, Feb 2024. URL: https://doi.org/10.1038/s41467-024-45525-3, doi:10.1038/s41467-024-45525-3. This article has 20 citations and is from a highest quality peer-reviewed journal.
(lei2024humanescderivedvascular pages 10-11): Jinghui Lei, Xiaoyu Jiang, Daoyuan Huang, Ying Jing, Shanshan Yang, Lingling Geng, Yupeng Yan, Fangshuo Zheng, Fang Cheng, Weiqi Zhang, Juan Carlos Izpisua Belmonte, Guang-Hui Liu, Si Wang, and Jing Qu. Human esc-derived vascular cells promote vascular regeneration in a hif-1α dependent manner. Protein & Cell, 15:36-51, May 2024. URL: https://doi.org/10.1093/procel/pwad027, doi:10.1093/procel/pwad027. This article has 14 citations and is from a peer-reviewed journal.
(zhou2019highankzf1expression pages 1-2): Xin Zhou, Yan-Na Shang, Ran Lu, Chuan-Wen Fan, and Xian-Ming Mo. High ankzf1 expression is associated with poor overall survival and recurrence-free survival in colon cancer. Jun 2019. URL: https://doi.org/10.2217/fon-2018-0920, doi:10.2217/fon-2018-0920. This article has 29 citations and is from a peer-reviewed journal.
(zhou2019highankzf1expression pages 2-4): Xin Zhou, Yan-Na Shang, Ran Lu, Chuan-Wen Fan, and Xian-Ming Mo. High ankzf1 expression is associated with poor overall survival and recurrence-free survival in colon cancer. Jun 2019. URL: https://doi.org/10.2217/fon-2018-0920, doi:10.2217/fon-2018-0920. This article has 29 citations and is from a peer-reviewed journal.
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