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🏛️ Indexed Academic JournalOriginal: 生物化学与生物物理学报

Acta Biochimica et Biophysica Sinica

Premier Chinese Biomedical Journal indexed in SinoBioData: Acta Biochimica et Biophysica Sinica (生物化学与生物物理学报).

Total Research Papers: 200
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Published Research PapersFiltered: Year 2025 • 57 • 4

Showing 3 of 200 peer-reviewed papers with full Graphical Abstracts.

Original ResearchVol. 57, Issue 4 • pp. 507-520DOI: 10.3724/abbs.2024228

Annexins: central regulators of plant growth and stress signaling

Authors: Chen Xie, Mingyue Zhu, Ruirui Shi, Liu Yang, Xiaoya An, Chao Wang

Annexins are a family of multifunctional calcium-dependent and phospholipid-binding proteins that are widely distributed in the plant kingdom. They have a highly conserved evolutionary history that dates back to single-celled protists. Plant annexins, as soluble proteins, can flexibly bind to endomembranes and plasma membranes, exhibiting unique calcium-dependent and calcium-independent characteristics. Members of the annexin family have diverse functions, including binding to F-actin, participating in ATP and GTP hydrolysis, and even serving as peroxidases or cation channels. Annexins play pivotal roles in plant growth and stress signaling. They can respond sensitively to environmental, metabolic, and developmental signals, thereby affecting cytoskeleton remodeling and exocytosis mechanisms. Plant annexin gene families have been successfully identified in multiple species, and their expression and intracellular localization are precisely regulated by developmental processes and environmental factors. Although research on plant annexins has aroused great interest, their depth and breadth still need further expansion compared with those of animal annexins. This article provides a comprehensive and in-depth review of the characteristics and functions of plant annexin families, revealing their core roles in plant growth and adaptation, and yielding valuable references and insights for future research.

Annexins: central regulators of plant growth and stress signaling
Graphical Abstract
Original ResearchVol. 57, Issue 4 • pp. 646-655DOI: 10.3724/abbs.2025027

Iron overload mediates cytarabine resistance in AML by inhibiting the TP53 signaling pathway

Authors: Yan Jia, Ling Li, Ying Li, Xunxun Zhu, Haiyan Wang, Bin Xu, Qiuping Li, Hao Zhang

Currently, chemotherapy remains the primary treatment for acute myeloid leukemia (AML). Drug resistance in AML cells is a critical factor contributing to the failure of chemotherapy remission and subsequent relapse. Iron overload frequently occurs in AML patients because of hematopoietic suppression or supportive blood transfusion therapy. Previous studies have indicated that iron overload may promote the progression of AML; however, the underlying mechanisms remain unclear. Our results demonstrate that, compared with TP53-wild-type AML cells, TP53-mutant AML cells exhibit increased resistance to cytarabine-induced cytotoxicity. Moreover, reducing TP53 expression in wild-type AML cells diminishes their sensitivity to cytarabine. The TP53 signaling pathway is essential for mediating cytarabine-induced apoptosis in AML cells. In this study, an iron overload model in AML cells via the use of ferric citrate is constructed. Our data indicate that iron overload can suppress the TP53/BCL2/BAX signaling pathway, counteracting cytarabine-induced apoptosis. In TP53 wild-type AML cells, TFR1 participates in iron-mediated resistance to cytarabine by regulating the entry of iron into the cells. These findings provide a foundation for further exploration of the molecular mechanisms involved in AML resistance to cytarabine.

Iron overload mediates cytarabine resistance in AML by inhibiting the TP53 signaling pathway
Graphical Abstract
Original ResearchVol. 57, Issue 4 • pp. 676-678DOI: 10.3724/abbs.2025009

Head-to-head: IL-21 triumphs over IL-15 in NK cell therapy for glioblastoma

Authors: Jake C. Miller, Bihui Cao, Jia Shen

Glioblastoma (GBM) is the most aggressive primary brain tumor. Despite current treatment options, including surgery, radiotherapy, and temozolomide chemotherapy, patient outcomes remain poor, with a median survival of less than 15 months. This dire prognosis highlights an urgent need to develop more effective therapies. Natural Killer (NK) cells, a key component of the innate immune system, are being actively investigated as a potential treatment for GBM. NK cells continually surveil their environment for abnormal cells, including GBM stem cells (GSCs), which are central to GBM progression and recurrence. While NK cells exhibit some ability to target GSCs independently, their activity can be significantly amplified by inflammatory cytokines. One such cytokine, interleukin-15 (IL-15), is critical for NK cell survival and function, making it a focal point of research in GBM immunotherapy. However, IL-15 is not without complications; it has been associated with toxicity, and its overexpression has been shown to induce leukemia in mouse models, potentially due to heightened inflammatory responses. These issues make IL-15 overexpression a less-than-ideal strategy for enhancing NK cell anti-tumor activity. To address these limitations, Shanley and colleagues recently identified interleukin-21 (IL-21) as a promising alternative to IL-15 in their study published in Cancer Cell. Their findings revealed that IL-21 overexpression provides prolonged NK cell activity, even under repeated exposure to GSCs, and demonstrates efficacy both in vitro and in vivo. Importantly, IL-21-expressing NK cells showed no significant toxicity when injected into mouse brains. These results suggest that IL-21 could represent a safer and more effective cytokine for boosting NK cell-mediated GBM therapy.

Head-to-head: IL-21 triumphs over IL-15 in NK cell therapy for glioblastoma
Graphical Abstract