Cited by 26Cell death mechanisms and regulationEndoplasmic Reticulum Stress and DiseaseHeat shock proteins research

NIBAN1, Exploring its Roles in Cell Survival Under Stress Context

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Diana, Paula, Carvalheira, Gianna Maria Griz·2022·Frontiers in Cell and Developmental Biology

Abstract

Cell survival must quickly activate specific mechanisms that enable to detect changes in the cellular microenvironment. The impact of these cell alteration has direct consequences on cellular homeostasis. Cellular stress, as well as its regulation and implication, has been studied in different pathologies. In this sense, the alteration in NIBAN1 expression seems to act in response to different cellular disturbances. Over the years, the knowledge of NIBAN1 functions has improved, demonstrating its important cell roles, favoring the cell survival under stress context. In response to the disturbances, NIBAN1 seems to be involved in the decision-making process between cell survival and death. The increase in NIBAN1 expression has been related to cellular mechanisms that seek to minimize the damage caused to cellular homeostasis. In this review, the main biological insights attributed to the NIBAN1 gene in different cellular contexts and its role as a mediator of cellular stress are discussed.

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Crossref · 10.3389/fcell.2022.867003

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  • All three microglial sub-populations showed upregulation of APOE, ATG16L2, BCL2, CCNH and GAS7; negative regulators of senescence GRB2 and NIBAN1 were downregulated with increasing β-amyloid.

    “All three microglial sub-populations showed upregulation of APOE, ATG16L2 (an autophagy antagonist gene), BCL2 (encoding a negative regulator of apoptosis), the CDK7 regulator gene CCNH and GAS7 (the growth arrest-specific protein 7 gene). Genes for negative regulators of senescence such as GRB2 and NIBAN1 were downregulated with increasing β-amyloid [17, 21, 34, 55].”

    From Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics (2024) · cites this paper as [17]

    The Cell Stress section (page unavailable) says NIBAN1 can suppress senescence in a prostate-cancer stress context, supporting its description as a negative regulator of senescence. It does not report NIBAN1 or GRB2 being downregulated as β-amyloid increases, or the stated expression changes across three microglial sub-populations. (LLM, conf=0.88)

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Authors
Diana, P., & Carvalheira, G. M. G.
Affiliations
Universidade Federal de São Paulo (BR)
Corresponding author
Carvalheira, Gianna Maria Griz
Venue
Frontiers in Cell and Developmental Biology
Published
2022-04-19
Volume
10
Pages
867003-867003
ISSN
2296-634X (ISSN-L)
OpenAlex
W4224298154
Cited by
26
References
73
Citations by year
2026: 5 · 2025: 7 · 2024: 10 · 2023: 4
FWCI
0.55
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Cell and Developmental Biology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (88882.430337/2019-01)
  • Fundação de Amparo à Pesquisa do Estado de São Paulo (2015/04164-3)
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico (470441/2013-5)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
Keywords
cell survival, cellular stress, cellular homeostasis, cell death, stress response, gene expression regulation

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