ArticleProceedings of the National Academy of Sciences of the United States of America2012
Transcription factor ATF5 is required for terminal differentiation and survival of olfactory sensory neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 52 citations in OpenAlex.
- CXCR4 Coordinates Long-Term Olfactory Epithelial Regeneration and Cellular Stress Response After Injury.Molecular neurobiology · 2026Article
- An epigenetic repressor TRIM66 dictates monogenic olfactory receptor expression, neural activity, and olfactory behavior.Nature communications · 2025Article
- Environmental stress promotes the persistence of juvenile traits in olfactory neurons as a protective mechanism.iScience · 2025Article
- Nescient helix-loop-helix 1 (Nhlh1) is a novel activating transcription factor 5 (ATF5) target gene in olfactory and vomeronasal sensory neurons in mice.Cell and tissue research · 2024Article
- Activating transcription factor 5 (ATF5) controls intestinal tuft and goblet cell expansion upon succinate-induced type 2 immune responses in mice.Cell and tissue research · 2023Article
- Molecular Evidence for Olfactory Neuroblastoma as a Tumor of Malignant Globose Basal Cells.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2023Article
- Evolution-driven crosstalk between glioblastoma and the tumor microenvironment.Cancer biology & medicine · 2023Article
- The mitochondrial UPR regulator ATF5 promotes intestinal barrier function via control of the satiety response.Cell reports · 2022Article
- Advancements in Activating Transcription Factor 5 Function in Regulating Cell Stress and Survival.International journal of molecular sciences · 2022Review
- Roles of mitochondrial unfolded protein response in mammalian stem cells.World journal of stem cells · 2021Review
- Mechanisms underlying pre- and postnatal development of the vomeronasal organ.Cellular and molecular life sciences : CMLS · 2021Review
- ATF5 deficiency causes abnormal cortical development.Scientific reports · 2021Article
- May the Odds Be Ever in Your Favor: Non-deterministic Mechanisms Diversifying Cell Surface Molecule Expression.Frontiers in cell and developmental biology · 2021Review
- The microRNA/TET3/REST axis is required for olfactory globose basal cell proliferation and male behavior.EMBO reports · 2020Article
- Expression patterns of activating transcription factor 5 (atf5a and atf5b) in zebrafish.Gene expression patterns : GEP · 2020Article
- Requirement of activating transcription factor 5 for murine fetal liver erythropoiesis.British journal of haematology · 2020Article
- Hop2 Interacts with ATF4 to Promote Osteoblast Differentiation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- Cardioprotection by the mitochondrial unfolded protein response requires ATF5.American journal of physiology. Heart and circulatory physiology · 2019Article
- Signaling and Regulation of the Mitochondrial Unfolded Protein Response.Cold Spring Harbor perspectives in biology · 2019Review
- Blood-brain barrier transport and neuroprotective potential of blackberry-digested polyphenols: an in vitro study.European journal of nutrition · 2019Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Activating transcription factor 5 (ATF5) is a member of the ATF/cAMP response element-binding family of transcription factors, which compose a large group of basic region leucine zipper proteins whose members mediate diverse transcriptional regulatory functions. ATF5 has a well-established prosurvival activity and has been found to be overexpressed in several human cancers, in particular glioblastoma. However, the role(s) of ATF5 in development and normal physiology are unknown. Here we address this issue by deriving and characterizing homozygous Atf5 knockout mice. We find that Atf5(-/-) pups die neonatally, which, as explained below, is consistent with an olfactory defect resulting in a competitive suckling deficit. We show that Atf5 is highly expressed in olfactory sensory neurons (OSNs) in the main olfactory epithelium starting from embryonic stage 11.5 through adulthood. Immunostaining experiments with OSN-specific markers reveal that ATF5 is expressed in some immature OSNs and in all mature OSNs. Expression profiling and immunostaining experiments indicate that loss of Atf5 leads to a massive reduction in mature OSNs resulting from a differentiation defect and the induction of apoptosis. Ectopic expression of Atf5 in neural progenitor cells induces expression of multiple OSN-specific genes. Collectively, our results suggest a model in which Atf5 is first expressed in immature OSNs and the resultant ATF5 functions to promote differentiation into mature OSNs. Thus, ATF5 is required for terminal differentiation and survival of OSNs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.