ArticleFrontiers in biology2015
Transcriptional regulation of secretory capacity by bZip transcription factors.
Article in Frontiers in biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- CREB3L1 Modulates Extracellular Matrix Gene Expression and Proliferation in Glaucomatous Lamina Cribrosa Cells.Biomedicines · 2026Article
- Identification and Characterization of theGenes · 2025Article
- MBTPS1: a membrane-bound transcription factor protease implicated in the pathogenesis of several skin and skeletal disorders.Functional & integrative genomics · 2025Review
- Gene module reconstruction identifies cellular differentiation processes and the regulatory logic of specialized secretion in zebrafish.Developmental cell · 2025Article
- Lack of Nuclear Localization of the Creb3l1 Transcription Factor Causes Defects in Caudal Fin Bifurcation in Zebrafish Danio rerio.Cells, tissues, organs · 2025Article
- The Regulatory Network of CREB3L1 and Its Roles in Physiological and Pathological Conditions.International journal of medical sciences · 2024Review
- Article
- NMP4, an Arbiter of Bone Cell Secretory Capacity and Regulator of Skeletal Response to PTH Therapy.Calcified tissue international · 2023Review
- Conditional Loss of Nmp4 in Mesenchymal Stem Progenitor Cells Enhances PTH-Induced Bone Formation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Article
- CREB3L2 Modulates Nerve Growth Factor-Induced Cell Differentiation.Frontiers in molecular neuroscience · 2021Article
- Regulation of autophagy by canonical and non-canonical ER stress responses.Seminars in cancer biology · 2020Review
- Cloning and Functional Analysis ofInternational journal of molecular sciences · 2020Article
- Pituitary cell translation and secretory capacities are enhanced cell autonomously by the transcription factor Creb3l2.Nature communications · 2019Article
- Golgi OncoproteinGenes · 2019Article
- Proteomics Study of Peripheral Blood Mononuclear Cells (PBMCs) in Autistic Children.Frontiers in cellular neuroscience · 2019Article
- CREB3 Transcription Factors: ER-Golgi Stress Transducers as Hubs for Cellular Homeostasis.Frontiers in cell and developmental biology · 2019Review
- Ulcerative colitis: functional analysis of the in-depth proteome.Clinical proteomics · 2019Article
- Elucidating post-translational regulation of mouse CREB3 in Neuro2a cells.Molecular and cellular biochemistry · 2018Article
- Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cells of specialized secretory organs expand their secretory pathways to accommodate the increased protein load necessary for their function. The endoplasmic reticulum (ER), the Golgi apparatus and the secretory vesicles, expand not only the membrane components but also the protein machinery required for increased protein production and transport. Increased protein load causes an ER stress response akin to the Unfolded Protein Response (UPR). Recent work has implicated several bZip transcription factors in the regulation of protein components of the early secretory pathway necessary to alleviate this stress. Here, we highlight eight bZip transcription factors in regulating secretory pathway component genes. These include components of the three canonical branches of the UPR-ATF4, XBP1, and ATF6, as well as the five members of the Creb3 family of transcription factors. We review findings from both invertebrate and vertebrate model systems suggesting that all of these proteins increase secretory capacity in response to increased protein load. Finally, we propose that the Creb3 family of factors may have a dual role in secretory cell differentiation by also regulating the pathways necessary for cell cycle exit during terminal differentiation.
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Registered trials
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.