Biochimica et biophysica acta. Molecular cell research最新文献_第2页

SFRP2 is involved in hyperoxia-induced bronchopulmonary dysplasia in newborn mice by suppressing Nrf2/HO-1 pathway. SFRP2通过抑制Nrf2/HO-1通路参与新生小鼠高氧诱导的支气管肺发育不良。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-05-18 DOI: 10.1016/j.bbamcr.2026.120157

Jingjing Li, Xiaoxia Feng, Ranran Si, Yuanyuan Liu, Zhifang Huo, Huanqing Song, Chuan Zhou

{"title":"SFRP2 is involved in hyperoxia-induced bronchopulmonary dysplasia in newborn mice by suppressing Nrf2/HO-1 pathway.","authors":"Jingjing Li, Xiaoxia Feng, Ranran Si, Yuanyuan Liu, Zhifang Huo, Huanqing Song, Chuan Zhou","doi":"10.1016/j.bbamcr.2026.120157","DOIUrl":"https://doi.org/10.1016/j.bbamcr.2026.120157","url":null,"abstract":"<p><p>Bronchopulmonary dysplasia (BPD), characterized by inflammation, is a severe pulmonary condition of preterm infants. This study aimed to investigate the role of secreted frizzled related protein 2 (SFRP2) in BPD and to elucidated its underlying mechanisms, focusing on inflammation, apoptosis, and the Nrf2/HO-1 signaling pathway. In vivo neonatal mouse models and in vitro murine lung epithelial-12 (MLE-12) models were established by hyperoxia induction. Administration of recombinant SFRP2 (rSFRP2) aggravated hyperoxia-induced lung injury, reduced alveolation, and increased inflammatory cytokines (TNF-α, IL-1β, and IL-6) in both lung tissues and cells (all P < 0.05). This demonstrated that SFRP2 aggravated hyperoxia-induced inflammation. These results were also evidenced by elevated numbers of inflammatory cells in the BALF and increasing counts of MAC-3 positive cells in the lung tissues of rSFRP2-treated BPD mice (all P < 0.05). rSFRP2 treatment promoted hyperoxia-induced apoptosis of lung tissue in mice and MLE-12 cells, reflected in increased count of TUNEL-positive cells. The Nrf2/HO-1 pathway was inhibited in the lung tissues of mice and MLE-12 cells after hyperoxia induction, and rSFRP2 therapy further suppressed its activity. Rescue experiments demonstrated that the activation of Nrf2 expression mitigated rSFRP2-induced inflammation and apoptosis in MLE-12 cells. Mechanically, SFRP2 promoted competitive binding of BACH1 to the ARE sequence of HO-1, impaired Nrf2 binding, and suppressed antioxidant signaling. We concluded that SFRP2 might exacerbate lung inflammation and apoptosis by inhibiting the Nrf2/HO-1 pathway, thus promoting the progression of BPD.</p>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":" ","pages":"120157"},"PeriodicalIF":3.7,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147970089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ADAM proteases in cytokine biology: Modulators of immune signaling, inflammation and cancer 细胞因子生物学中的ADAM蛋白酶：免疫信号、炎症和癌症的调节剂。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-04-01 Epub Date: 2026-03-22 DOI: 10.1016/j.bbamcr.2026.120137

Heba Khattab , Jelena Solujic , Mohamed I. Saad

{"title":"ADAM proteases in cytokine biology: Modulators of immune signaling, inflammation and cancer","authors":"Heba Khattab , Jelena Solujic , Mohamed I. Saad","doi":"10.1016/j.bbamcr.2026.120137","DOIUrl":"10.1016/j.bbamcr.2026.120137","url":null,"abstract":"<div><div>Ectodomain shedding, a post-translational process mediated primarily by A Disintegrin And Metalloprotease (ADAM) family members, represents a fundamental mechanism regulating intercellular communications. By cleaving the extracellular domains of membrane-anchored cytokines, receptors, growth factors, and adhesion molecules, ADAM proteases dynamically shape cytokine signaling networks that underpin immune regulation, inflammation, and tissue homeostasis. Among these enzymes, ADAM10 and ADAM17 are key effectors whose tightly controlled activity ensures the fine-tuning of pro- and anti-inflammatory pathways. Dysregulated ADAM function perturbs cytokine gradients and receptor availability, contributing to the pathogenesis of cancer, autoimmune disorders, and chronic inflammatory diseases. In this review, we provide updated perspectives on the mechanisms governing ADAM activation and substrate selectivity, including prodomain processing, trafficking, interaction with protein partners, and modulation by inflammatory stimuli. We further highlight species-specific differences and genetic polymorphisms that influence ADAM expression and catalytic efficiency, emphasizing their translational relevance in precision medicine. Collectively, delineating the ADAM/cytokine signaling axis offers crucial insights into immune homeostasis and unveils novel opportunities for therapeutic intervention in cancer and immune-mediated diseases.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 4","pages":"Article 120137"},"PeriodicalIF":3.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pathogenic implication of the CD53 tetraspanin in immune and cancer cells CD53蛋白在免疫细胞和癌细胞中的致病意义。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-04-01 Epub Date: 2026-03-30 DOI: 10.1016/j.bbamcr.2026.120142

Pedro A. Lazo

{"title":"Pathogenic implication of the CD53 tetraspanin in immune and cancer cells","authors":"Pedro A. Lazo","doi":"10.1016/j.bbamcr.2026.120142","DOIUrl":"10.1016/j.bbamcr.2026.120142","url":null,"abstract":"<div><div>Tetraspanin proteins are a specific family of membrane proteins with four transmembrane domains forming a core that assembles different types of complexes by their interactions among themselves, and with other membrane, extracellular and intracellular proteins. These tetraspanin complexes modulate multiple signaling pathways and generate exosomes. Tetraspanin proteins have a heterogeneous distribution, some are expressed in many different cell types, while others are highly restricted to specific cell types. Among the latter is CD53 (TSPAN25), a tetraspanin protein that is mainly expressed in nucleated hematopoietic cells, although it has also been detected in some carcinomas. CD53 forms oligomeric complexes with other members of this protein family in cell membranes, which can assemble and release exosomes and intracellular vesicles. CD53 on the plasma membrane modulates cell adhesion, migration, cell proliferation and survival. CD53 has no known specific ligand, but its ligation with specific antibodies modulates different intracellular signals, among which is protecting cells from apoptosis that is mediated by phosphorylation and activation of Akt, increased Bcl-xL level, decreased Bax level, and reducing caspase activation. CD53 ligation also induces calcium mobilization, activation of PKC and DREAM complex, and expression of the inducible nitric oxide synthase gene resulting in increased nitric oxide production. The different biological roles of CD53 are implicated in the regulation of specific functions associated with both immune responses and tumor biology. However, the heterogeneity of the cell types and of the pathways in which CD53 participates need to be studied in combination with other tetraspanins in order to detect their cooperation and contribution in specific cell types, normal or tumoral.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 4","pages":"Article 120142"},"PeriodicalIF":3.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147589497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Signal peptide-directed proteins generated in the endoplasmic reticulum are secreted or degraded via the autophagic pathway 内质网中产生的信号肽导向蛋白通过自噬途径分泌或降解。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-04-01 Epub Date: 2026-03-27 DOI: 10.1016/j.bbamcr.2026.120140

Taek-Yeong Kim, Ye-Jin Cho, Kwon-Yul Ryu

{"title":"Signal peptide-directed proteins generated in the endoplasmic reticulum are secreted or degraded via the autophagic pathway","authors":"Taek-Yeong Kim, Ye-Jin Cho, Kwon-Yul Ryu","doi":"10.1016/j.bbamcr.2026.120140","DOIUrl":"10.1016/j.bbamcr.2026.120140","url":null,"abstract":"<div><div>Signal peptides (SPs) are short N-terminal sequences that direct proteins to the endoplasmic reticulum (ER). After cleavage of the SP, these proteins are mostly trafficked to the Golgi apparatus for secretion. Lipocalin-2 (LCN2), a neurotoxic secretory protein, was recently identified as a target of autophagy. The presence of an SP is a prerequisite for secretion and autophagic degradation. Based on these observations, we investigated whether the SP of LCN2 is sufficient to enable proteins to be secreted or degraded via autophagy. We fused the SP of LCN2 to a non-secretory green fluorescent protein (GFP) and found that this ER-generated GFP was either secreted or degraded via autophagy. These results indicate that the LCN2-derived SP alone is sufficient to direct proteins to the ER and subsequent secretion or autophagic degradation. This dual regulation was abolished when the SP was deleted from LCN2. Notably, the effect was preserved even when the LCN2 SP was replaced with the SP from brain-derived neurotrophic factor, another secretory protein. These results suggest that SPs with different sequences can similarly direct proteins to the ER and subsequent secretion or autophagic degradation. Furthermore, we found that even when LCN2 reached the Golgi apparatus for secretion, it could also be degraded via autophagy. Thus, we propose that SP-directed and ER-generated secretory proteins can undergo autophagic degradation during ER-Golgi transport, including at the ER, the ER-Golgi intermediate compartment, or the Golgi apparatus. Taken together, degradation of secretory proteins via autophagy suggests implications for the potential control of secretory protein homeostasis.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 4","pages":"Article 120140"},"PeriodicalIF":3.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147572053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Interaction of estrogen and interleukin 6 in the progression of lymphangioleiomyomatosis 雌激素和白细胞介素6在淋巴管平滑肌瘤病进展中的相互作用

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-04-01 Epub Date: 2026-03-31 DOI: 10.1016/j.bbamcr.2026.120143

Lulu Yang , Liting Huang , Siying Ren

{"title":"Interaction of estrogen and interleukin 6 in the progression of lymphangioleiomyomatosis","authors":"Lulu Yang , Liting Huang , Siying Ren","doi":"10.1016/j.bbamcr.2026.120143","DOIUrl":"10.1016/j.bbamcr.2026.120143","url":null,"abstract":"<div><div>Lymphangioleiomyomatosis (LAM) is an estrogen-dependent disease that promotes tumor cell growth through estrogen receptor α (ERα). Interleukin 6 (IL-6) is an important estrogen (E2) target gene; however, its role in disease progression remains unclear. In the present study, we investigated the biological functions and underlying mechanisms of action of IL-6 in E2-stimulated tuberous sclerosis complex 2 (TSC2)–deficient cells. The IL-6 levels in the lung tissue and serum of the patients were detected using immunohistochemistry and enzyme-linked immunosorbent assay (ELISA). The effects of E2 and recombinant IL-6 on ERα and IL-6 signaling and the malignant behaviors of TSC2-deficient cells were examined using western blotting, immunofluorescence, Cell Counting Kit-8 (CCK-8), colony formation, transwell, and wound healing assays. The IL-6 expression was higher in LAM lung tissues than in controls, was significantly elevated in the serum of patients with LAM, and was negatively correlated with lung function. After E2 and recombinant human IL-6 (rhIL-6) intervention in TSC2-deficient cells, the expression of IL-6 and ERα was upregulated in a time-dependent manner. Fulvestrant treatment had no significant inhibitory effect on IL-6 protein expression, whereas Stattic intervention inhibited ERα expression. The combined use of fulvestrant and Stattic significantly suppressed the proliferation and migration of TSC2-deficient cells, indicating that the IL-6/signal transducer and activator of transcription 3 (STAT3) pathway plays an important role in E2-promoted LAM progression and may serve as a potential therapeutic target for LAM.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 4","pages":"Article 120143"},"PeriodicalIF":3.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147600604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ADAR1 upregulates the translation of cytochrome c via the inhibition of translocation into stress granules, facilitating apoptosis by an anticancer agent ADAR1通过抑制细胞色素c转运到应激颗粒中来上调细胞色素c的翻译，促进抗癌药物的凋亡。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-03-01 Epub Date: 2026-01-06 DOI: 10.1016/j.bbamcr.2025.120104

Motoki Isono , Tomoka Yamakawa , Kyoka Nagaoka , Masataka Nakano , Tatsuki Fukami , Miki Nakajima

{"title":"ADAR1 upregulates the translation of cytochrome c via the inhibition of translocation into stress granules, facilitating apoptosis by an anticancer agent","authors":"Motoki Isono , Tomoka Yamakawa , Kyoka Nagaoka , Masataka Nakano , Tatsuki Fukami , Miki Nakajima","doi":"10.1016/j.bbamcr.2025.120104","DOIUrl":"10.1016/j.bbamcr.2025.120104","url":null,"abstract":"<div><div>Adenosine-to-inosine (A-to-I) RNA editing catalyzed by adenosine deaminase acting on RNA (ADAR) 1 is the most abundant RNA modification in humans. We noticed that there are multiple A-to-I RNA editing sites in the 3′-UTR of cytochrome <em>c</em> (CYCS), a mitochondrial protein involved in the initiation of apoptosis. We aimed to clarify the impact of ADAR1 on the regulation of CYCS expression, its mechanism, and its biological and pharmacological significance. In human hepatocellular carcinoma-derived HepG2 or Huh-7 cells, siRNA-mediated knockdown of ADAR1 (siADAR1) reduced CYCS protein levels without affecting mRNA levels, suggesting that ADAR1 facilitates CYCS translation. Sanger sequence analysis showed that multiple adenosines in the 3′-UTR of CYCS are highly edited by ADAR1. The CYCS protein level in HepG2 <sup><em>CYCS 3′-UTR-deleted</em></sup> cells in which the 3′-UTR of CYCS was deleted by the CRISPR/Cas9 system was not decreased by siADAR1, indicating that the 3′-UTR is required for ADAR1-dependent translational regulation. The pulldown assay revealed that siADAR1 increases the binding of CYCS mRNA to RNA-binding proteins with disordered regions, suggesting that stress granules, a membrane-less organelle formed by such proteins with intrinsically disordered regions, might trap CYCS mRNA and suppress its translation. Treatment with ISRIB, an inhibitor of stress granule formation, attenuated the siADAR1-mediated decrease in CYCS protein levels. Interestingly, sorafenib-induced apoptosis in HepG2 cells was repressed by siADAR1, but this repression was not observed in HepG2 <sup><em>CYCS 3′-UTR-deleted</em></sup> cells. Collectively, this study clarified that ADAR1 upregulates CYCS translation by inhibiting stress granule formation and thereby can facilitate anticancer agent-induced apoptosis.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 3","pages":"Article 120104"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145931913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Insights from Interleukin-6 trans-signaling and implications for the control of cytokine activity 白细胞介素-6反式信号传导及其对细胞因子活性控制的意义。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-03-01 Epub Date: 2026-01-09 DOI: 10.1016/j.bbamcr.2026.120109

Stefan Rose-John

引用次数: 0

Understanding complex formation of gp130 cytokines for the design of selective therapeutics 了解gp130细胞因子的复杂形成以设计选择性疗法。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-03-01 Epub Date: 2026-01-05 DOI: 10.1016/j.bbamcr.2026.120105

Isabel Ramón Roth , Jana I. Führing , Christoph Garbers

{"title":"Understanding complex formation of gp130 cytokines for the design of selective therapeutics","authors":"Isabel Ramón Roth , Jana I. Führing , Christoph Garbers","doi":"10.1016/j.bbamcr.2026.120105","DOIUrl":"10.1016/j.bbamcr.2026.120105","url":null,"abstract":"<div><div>Cytokines activate their target cells via binding to specific receptors on the cell surface. The receptor glycoprotein 130 (gp130) is ubiquitously expressed throughout the human body and used by nine members of the interleukin-6 (IL-6) family of cytokines to facilitate the initiation of intracellular signalling cascades. Although these cytokines share the same protein fold, gp130 requires substantial promiscuity in order to bind such diverse proteins. In this review, we summarize what is currently known about the structural features of gp130 that allow this flexibility towards its binding partners. We compare this to the other non-signalling α-receptors and signal-transducing β-receptors of the family and discuss how IL-6 family cytokines form signalling complexes at the cell surface that lead to the activation of intracellular signalling cascades. We further show how mutations found in human patients influence gp130 signalling, and describe how such knowledge can be used to create tailor-made designer proteins that can be used as next-generation therapeutics for the treatment of inflammatory diseases.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 3","pages":"Article 120105"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145916918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cyclin dependent kinases CDK8/19 are required for PKA inactivation during meiosis resumption 细胞周期蛋白依赖激酶CDK8/19是PKA在减数分裂恢复过程中失活所必需的。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-03-01 Epub Date: 2026-01-17 DOI: 10.1016/j.bbamcr.2026.120114

Yulia Okulova , Maxim Filatov , Ekaterina Varlamova , Anna Tvorogova , Evgeniy Korshunov , Yulia Silaeva , Victor Tatarskiy , Alexandra Bruter

{"title":"Cyclin dependent kinases CDK8/19 are required for PKA inactivation during meiosis resumption","authors":"Yulia Okulova , Maxim Filatov , Ekaterina Varlamova , Anna Tvorogova , Evgeniy Korshunov , Yulia Silaeva , Victor Tatarskiy , Alexandra Bruter","doi":"10.1016/j.bbamcr.2026.120114","DOIUrl":"10.1016/j.bbamcr.2026.120114","url":null,"abstract":"<div><div>CDK8/19 are transcriptional cyclin dependent kinases, which do not directly control cell cycle progression. CDK8/19 are involved in regulation of multiple processes in embryogenesis, cancer progression, immune activation and others. Previously we demonstrated that CDK8/19 are critical for spermatogenesis in mice. Here we report that CDK8/19 activity is also required for oocyte maturation playing a significant role in meiosis resumption in mouse oocytes. Two chemically distinct CDK8/19 inhibitors – Senexin B and Snx631 prevented nuclear envelope breakdown and first polar body extrusion, blocking key molecular events required for exiting the dictyate - inhibition of PKA activity and activation of the CDK1/Cyclin B complex. This effect did not cause cytotoxicity, and oocytes could resume progression upon transfer into fresh media. Inhibition of CDK8/19 also prevented meiotic-specific mitochondrial expansion and clustering. Notably, these effects appear to be independent of roles of CDK8/19 in transcription, which is not required for resumption of meiosis. These findings for the first time demonstrate the roles of CDK8/19 activity in oocyte maturation, through its role in transcription-independent regulation of PKA activity.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 3","pages":"Article 120114"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146002960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Insights into the regulation and signaling landscape of cardiotrophin-like cytokine factor 1 (CLCF1) 心肌营养因子样细胞因子1 （CLCF1）的调控和信号转导研究。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-03-01 Epub Date: 2026-02-07 DOI: 10.1016/j.bbamcr.2026.120123

Marine Rousseau , France Côté , Sylvain Chemtob , Jean-François Gauchat , Sarah Pasquin , Sylvie Lesage

{"title":"Insights into the regulation and signaling landscape of cardiotrophin-like cytokine factor 1 (CLCF1)","authors":"Marine Rousseau , France Côté , Sylvain Chemtob , Jean-François Gauchat , Sarah Pasquin , Sylvie Lesage","doi":"10.1016/j.bbamcr.2026.120123","DOIUrl":"10.1016/j.bbamcr.2026.120123","url":null,"abstract":"<div><div>Cardiotrophin-like cytokine factor 1 (CLCF1) is an essential gene that shows exceptional sequence conservation among vertebrates. <em>CLCF1</em> loss-of-function mutations cause Crisponi/cold-induced sweating syndrome-2, a disorder with severe and complex phenotypes, underscoring the non-redundant roles of CLCF1. Initially identified as a member of the interleukin-6 (IL-6) cytokine family with activity in neurons and immune cells, CLCF1 is now recognized for broader roles in thermoregulation, glomerular function, myelopoiesis, oncogenesis, and muscle fitness. Despite growing interest in the multifaceted biology of CLCF1, the mechanisms regulating its transcription, translation, secretion, receptor binding, and signaling remain incompletely understood. This review integrates data from multiple open databases and functional studies to outline the current state of knowledge regarding CLCF1 regulatory landscape, receptor interactions, and downstream signaling. It also highlights recent discoveries about the CLCF1 interactome and intracellular functions and underlines its emerging potential as a therapeutic target.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 3","pages":"Article 120123"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146148935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0