Biochemical And Biophysical Research Communications[JOURNAL]
Sun
200 papers
Residue interaction chains facilitating the structural change of ND6 subunit in respiratory complex I.
Shibata M, Kuramitsu Y, Matsuura ET … +2 more , Kondo R, Yura K
Biochem Biophys Res Commun · 2026 Jun · PMID 42365826 · Publisher ↗
Respiratory complex I generates proton gradient through coupled NADH: ubiquinone oxidoreduction and proton pumping for ATP synthesis in aerobic respiration. Structural studies showed the involvement of the third transmem...
Respiratory complex I generates proton gradient through coupled NADH: ubiquinone oxidoreduction and proton pumping for ATP synthesis in aerobic respiration. Structural studies showed the involvement of the third transmembrane helix in ND6 subunit (TMH3) in the global open-closed conformational change of RCI was important for the functional coupling. However, the atomistic mechanism for the conformational change of TMH3 remains unclear. Here, we computationally analyzed the network graphs of coevolving residue contacts of the core functional subunits derived from Escherichia coli and Ovis aries. We identified four conserved paths connecting the quinone-binding site and TMH3. Together with structural frustration and genomic variant analyses, we suggest that these paths can transmit structural disturbance upon quinone binding, facilitating the conformational change of TMH3.
CD206 deficiency aggravates paraquat-induced acute lung injury in mice.
Yamashita M, Yasuno W, Niisato M … +4 more , Kawasaki Y, Kwon E, Ito S, Kawada I
Biochem Biophys Res Commun · 2026 Jun · PMID 42365825 · Publisher ↗
Paraquat induces acute lung injury characterized by oxidative epithelial damage. To examine the role of CD206, we compared C57BL/6J wild-type and CD206-deficient mice after paraquat exposure. CD206 deficiency increased m...
Paraquat induces acute lung injury characterized by oxidative epithelial damage. To examine the role of CD206, we compared C57BL/6J wild-type and CD206-deficient mice after paraquat exposure. CD206 deficiency increased mortality, body weight loss, bronchoalveolar lavage protein, total cells, histological fibrosis scores, and 8-OHdG levels, together with reduced Hmox1 expression in alveolar macrophages. In co-culture experiments, CD206-deficient monocyte-derived macrophages enhanced epithelial cell death compared with wild-type macrophages, whereas N-acetylcysteine restored epithelial survival. These findings identify a previously unrecognized role for CD206 in macrophage-associated epithelial protection during acute oxidant lung injury.
Synthesising lithium-alumina-borate glass-ceramic for potential applications in regenerative bone establishment.
Ridzuan D, Ahmad NE, Mohd Noor SNF
Biochem Biophys Res Commun · 2026 Jun · PMID 42364322 · Publisher ↗
Lithium-alumina-borate (LAB) glass-ceramic demonstrates potential materials with physicochemical and cytocompatibility characteristics which needs further investigation in terms of bone regeneration. Borate substitution...
Lithium-alumina-borate (LAB) glass-ceramic demonstrates potential materials with physicochemical and cytocompatibility characteristics which needs further investigation in terms of bone regeneration. Borate substitution in the LAB follows the formula in mole percentages (mol.%) of 70 BO-(30-x) LiO-x AlO. The melt-derived LAB was dried at 60 °C and subjected to thermal analysis, X-ray powder diffraction (XRD) analysis, Fourier transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM) with energy-dispersive X-ray (EDX) spectroscopy, pH profile analysis and in vitro bioactivity using simulated body fluid (SBF) with biocompatibility assessment towards SaOS-2 human cell line. Thermal analysis confirmed the stability and glass-forming ability of LAB glass-ceramic. The XRD showed peaks corresponding to HA for LA4B and LA6B at 2θ degree, ranging from 20° to 60°, while FTIR showed phosphate peaks of hydroxyapatite overlapping with the borate or alumina peaks for LA4B and LA6B at ∼550 cm and ∼1100 cm. SEM-EDX results showed that LA4B samples formed better HA than LA6B and LA8B because the former has more phosphorus and calcium deposition in weight percentages on the glass-ceramic surface than the latter. The pH profiles of all the LAB glass-ceramic showed increasing trends until day 7, thereby suggesting potential HA formation. The in vitro ionic release in SBF advocates the role of each element in LAB because of its bioactive and biocompatible characteristics. MTT assays elucidate the potential of LA4B samples to be biocompatible towards the human osteoblast SaOS-2 and a cytocompatibility candidate that merits further biological evaluation, including osteogenic differentiation and in vivo studies, before its suitability for bone regeneration can be established.
A coelenterazine-dependent luciferase from the deep-sea coral Anthoptilum murrayi.
Galeazzo GA, Soares DMM, Amaral DT … +6 more , Sartorelli P, Silva ACLN, Samuels E, Melo MRS, Stevani CV, Oliveira AG
Biochem Biophys Res Commun · 2026 Jun · PMID 42364321 · Publisher ↗
Bioluminescence is visible light produced by living organisms through luciferase-catalyzed oxidation of luciferins. Although widespread in anthozoans, the molecular basis of their light emission remains poorly defined. C...
Bioluminescence is visible light produced by living organisms through luciferase-catalyzed oxidation of luciferins. Although widespread in anthozoans, the molecular basis of their light emission remains poorly defined. Characterization has focused onRenilla reniformis, leaving anthozoan luciferase diversity underexplored. Here, we report the identification and characterization of a coelenterazine-dependent luciferase from the Murray's sea pen Anthoptilum murrayi (AnmLuc). Transcriptome analysis identified a transcript encoding a ∼35-kDa protein with characteristic motifs. The coding sequence was cloned and the recombinant protein was expressed in Escherichia coli. The reaction catalyzed by the purified enzyme resulted in an intense blue light emission (λ≈ 495 nm) in the presence of coelenterazine, with an activity optimum near 15 °C and 30-40% of maximal activity still measurable at 2-5 °C. These findings provide the first molecular characterization of a deep-sea anthozoan luciferase, expanding known diversity, and offering insights into Anthozoan light emission.
SLC5A2-SRC-ERK/STAT3 signaling network in proximal tubule S1 cells mediates the renoprotective effects of dapagliflozin in obese mice.
Sun F, Cai J, Zhao S … +8 more , Pan Q, Yang F, Wang D, Tan R, Dong F, Wang S, Liu W, Yan Y
Biochem Biophys Res Commun · 2026 Jun · PMID 42364320 · Publisher ↗
Obesity-related kidney disease (ORKD) has a complex pathogenesis, and current therapeutic strategies have significant limitations. Although sodium-glucose cotransporter 2 inhibitors (SGLT2i) exhibit remarkable renoprotec...
Obesity-related kidney disease (ORKD) has a complex pathogenesis, and current therapeutic strategies have significant limitations. Although sodium-glucose cotransporter 2 inhibitors (SGLT2i) exhibit remarkable renoprotective effects, their direct cellular targets and underlying molecular mechanisms remain unclear. In this study, we systematically elucidated the mechanism of action of dapagliflozin (DAPA) by integrating a high-fat diet (HFD)-induced obese mouse model, single-nucleus RNA sequencing (snRNA-seq), high-dimensional gene co-expression network analysis (hdWGCNA), in vitro functional validation, and urinary metabolomics. We identified the S1 segment of the proximal tubule (PT-S1) as the core cell type mediating the response to obesity-induced stress and drug-mediated renoprotection. Under obese conditions, the expression of sodium-glucose cotransporter 2 (SGLT2), encoded by the solute carrier family 5 member 2 (SLC5A2) gene, was aberrantly upregulated in this cell subset. Acting as a central signaling hub, SLC5A2 activates SRC kinase, which in turn triggers the phosphorylation of the downstream extracellular regulated protein kinases 1/2 (ERK1/2) and signal transducer and activator of transcription 3 (STAT3) signaling cascades, thus forming a synergistically amplified injury network that ultimately leads to impaired renal intercellular communication and systemic metabolic imbalance. By directly targeting and inhibiting SLC5A2, DAPA blocked the aberrant activation of this cooperative network at its source, restored the expression of key paracrine signaling molecules (VEGFA, vascular endothelial growth factor A; COL4A4, collagen type IV alpha 4 chain), remodeled the renal tissue microenvironment, and reversed the dysregulation of systemic oxidative stress-related metabolites and the aldosterone signaling pathway. At single-cell resolution, this study delineated a novel mechanism underlying the multidimensional renoprotective effects of SGLT2i, mediated through interference with the SLC5A2-SRC-ERK/oxidative stress-STAT3 cooperative signaling network, thereby laying a new theoretical foundation for the clinical application of SGLT2i in the management of ORKD.
Research progress on the association between diabetes mellitus and risk of cancer: From epidemiology to molecular mechanisms.
Huang Y, Ju S, Li S
Biochem Biophys Res Commun · 2026 Jun · PMID 42364319 · Publisher ↗
Diabetes mellitus and cancer represent two major global health burdens. This paper systematically reviews and analyzes recent research advances on the relationship between diabetes and cancer risk, encompassing both epid...
Diabetes mellitus and cancer represent two major global health burdens. This paper systematically reviews and analyzes recent research advances on the relationship between diabetes and cancer risk, encompassing both epidemiological and molecular mechanism studies. Epidemiological data indicate that the association between diabetes and cancer exhibits significant organ specificity, geographic and population variability, as well as type-specific differences. Diabetes mellitus significantly increases the risk of hepatocellular carcinoma, pancreatic cancer, breast cancer, and colorectal cancer, yet exhibits a unique inverse association with prostate cancer risk. At the molecular level, hyperinsulinemia directly promotes tumor cell proliferation by activating the PI3K/AKT/mTOR and Ras/MAPK/ERK signaling pathways through the insulin/IGF-1 axis. Concurrently, hyperglycemia creates a favorable microenvironment for tumorigenesis by enhancing the Warburg effect, promoting advanced glycation end-product (AGE) accumulation, and inducing oxidative stress and chronic inflammation. Beyond the classical pathways of hyperinsulinemia and hyperglycemia in diabetes, recent research has explored novel directions, including tumor microenvironment remodeling, epigenetics, and immunometabolism. These discoveries encompass emerging mechanisms such as exosomes acting as long-range messengers of systemic metabolic disorders, novel key signaling molecules (e.g., inhibin subunit βB (INHBB) and fibrinogen C domain containing 1 (FIBCD1)), and the remodeling of Schwann cells within the tumor microenvironment. These mechanisms, coupled with potential intervention targets like INHBB, glioma-associated oncogene 1 (Gli-1), FIBCD1, and estrogen-related receptor alpha (ERRα), offer novel clinical approaches for tumor screening, treatment, and prevention.
Integrative analysis of machine learning and single-cell sequencing identifies IGHG1 as a therapeutic target for epimedium in diabetes-gastric cancer comorbidity.
Tang D, Yao H, Bao W … +5 more , Zhai Y, Li Q, Zhao Y, Zhou W, Wu W
Biochem Biophys Res Commun · 2026 Jun · PMID 42364318 · Publisher ↗
BACKGROUND: The clinical comorbidity of diabetes mellitus (DM) and gastric cancer (GC) presents a significant healthcare challenge, as these two conditions often synergistically promote disease progression. Although Epim...
BACKGROUND: The clinical comorbidity of diabetes mellitus (DM) and gastric cancer (GC) presents a significant healthcare challenge, as these two conditions often synergistically promote disease progression. Although Epimedium is known for its anti-tumor and metabolic regulatory properties, the precise molecular mechanism by which it intervenes in the DM-GC comorbidity remains poorly understood. METHODS: We integrated transcriptomic datasets of DM and GC to identify common differentially expressed genes (DEGs). Machine learning algorithms, enhanced by SHapley Additive exPlanations (SHAP) analysis, were utilized to isolate core genes within both disease contexts. These candidates were then intersected with the predicted targets of Epimedium. To refine the targets, single-cell RNA sequencing (scRNA-seq) analysis was performed to evaluate cell-specific expression patterns. Additionally, CCK-8, Western blot, and qPCR assays were conducted in human HGC-27 cells to validate the therapeutic efficacy of Epimedium in vitro. RESULTS: Eight common DEGs were identified, leading to the selection of GABRA1 and IGHG1 as primary hub genes. scRNA-seq analysis revealed that IGHG1 was significantly overexpressed in GC tissues compared to normal tissues, particularly within the B-cell population, whereas GABRA1 showed insufficient expression levels for further analysis. In cellular verification, HGC-27 cell viability was significantly inhibited by Epimedium in a dose-dependent manner, with a half-maximal inhibitory concentration (IC50) of 632.3 μg/ml. Furthermore, the expression of IGHG1 was markedly downregulated at both the transcriptional and translational levels following Epimedium treatment. CONCLUSIONS: Our findings identify IGHG1 as a critical molecular bridge in the DM-GC comorbidity. Epimedium exerts potent anti-tumor effects by targeting and downregulating IGHG1 expression. This study provides a novel therapeutic strategy and a robust theoretical basis for the treatment of patients suffering from concurrent diabetes and gastric cancer.
Glycation stress induced by glyceraldehyde promotes vimentin accumulation and disrupts aggresome clearance in Hep3B cells.
Sakai-Sakasai A, Takeda K, Takeuchi M
Biochem Biophys Res Commun · 2026 Jun · PMID 42361745 · Publisher ↗
Vimentin plays a critical role not only as a cytoskeletal protein, but also in stress responses; however, its relationship with glycation stress remains unclear. Therefore, we herein investigated the behavior of vimentin...
Vimentin plays a critical role not only as a cytoskeletal protein, but also in stress responses; however, its relationship with glycation stress remains unclear. Therefore, we herein investigated the behavior of vimentin and its impact on proteostasis under glycation stress conditions induced by glyceraldehyde (GA), a potent precursor of advanced glycation end-products (AGEs), using human hepatic Hep3B cells. Upon proteasome inhibition, ubiquitinated misfolded proteins were previously shown to accumulate and form aggresomes in the perinuclear region, around which vimentin assembled into cage-like structures. In the present study, vimentin accumulated in the perinuclear region of GA-treated cells, whereas ubiquitinated proteins did not accumulate or form aggresomes. The accumulation of vimentin in GA-treated cells was associated with AGE-dependent cross-linking and persisted even after the removal of GA. In addition to these changes in vimentin itself, the GA treatment impaired the clearance of aggresomes that formed under the MG132 treatment. The partial restoration of aggresome clearance upon the knockdown of vimentin suggests that vimentin is, at least in part, involved in this inhibitory effect. These results indicate that GA induces the accumulation of vimentin and may affect proteostasis by inhibiting aggresome clearance, providing novel insights into the effects of glycation stress on hepatocytes.
Crystal structure of a LysR regulator reveal an unconventional effector pocket from Acinetobacter baumannii.
Lu Q, Hu B, Yu Y … +5 more , Xu Y, Qian X, Ge H, Ma J, Wang N
Biochem Biophys Res Commun · 2026 Jun · PMID 42361744 · Publisher ↗
Acinetobacter baumannii is a multidrug-resistant pathogen, and rising chlorhexidine tolerance threatens infection control. chlorhexidine induces the AceI efflux pump via the transcriptional regulator AceR, but the struct...
Acinetobacter baumannii is a multidrug-resistant pathogen, and rising chlorhexidine tolerance threatens infection control. chlorhexidine induces the AceI efflux pump via the transcriptional regulator AceR, but the structural basis of effector recognition by AceR is unknown. Here, we report the 1.82 Å crystal structure of the AceR effector-binding domain (EBD) and its co-crystal structure with spermidine, a physiological substrate. A clear spermidine density appeared at the homodimer interface, where the ligand is symmetrically coordinated by both protomers-an arrangement seldom seen in LTTR family. Site-directed mutagenesis combined with isothermal titration calorimetry (ITC) demonstrates that amino acid substitutions at this interface impair CHX binding, confirming its physiological relevance. These results reveal an unconventional ligand-binding site at the AceR homodimer interface, expanding the LTTR regulatory paradigm and identifying a novel pocket.
Dysregulation of ATP6V1B1 in renal intercalated cells in the pathophysiology of type 4 renal tubular acidosis.
Tomomitsu Y, Ishizawa K, Kuribayashi-Okuma E … +1 more , Shibata S
Biochem Biophys Res Commun · 2026 Jun · PMID 42361743 · Publisher ↗
Type 4 renal tubular acidosis (RTA) is a common disorder characterized by hyperkalemic non-anion gap metabolic acidosis. Although type 4 RTA is generally attributed to impaired renal ammoniagenesis induced by hyperkalemi...
Type 4 renal tubular acidosis (RTA) is a common disorder characterized by hyperkalemic non-anion gap metabolic acidosis. Although type 4 RTA is generally attributed to impaired renal ammoniagenesis induced by hyperkalemia, whether defects in distal nephron acidification contribute to its pathophysiology remains unclear. Here, we investigated alterations in distal nephron acidification machinery in Kelch-like 3 knock-in (KLHL3-KI) mice, a genetically engineered model of pseudohypoaldosteronism type II. KLHL3-KI mice exhibited hyperkalemia, hyperchloremia, and reduced serum bicarbonate levels, consistent with type 4 RTA. Phosphoenolpyruvate carboxykinase (PEPCK), a key enzyme involved in proximal tubular ammoniagenesis, was significantly reduced in KLHL3-KI mice as compared with wild-type mice. In addition, ATP6V1B1, a subunit of the vacuolar H-ATPase selectively expressed in intercalated cells, was significantly decreased in membrane fraction. Renal medullary expression of Rh C glycoprotein (RHCG), a major ammonia transporter in the distal nephron, was also reduced. To determine whether these changes were secondary to hyperkalemia, KLHL3-KI mice were fed a low-K diet. Correction of hyperkalemia with a low-K diet significantly increased RHCG abundance, whereas ATP6V1B1 levels remained unchanged. By immunostaining, we found that WNK1 bodies were detected in a subset of ATP6V1B1-positive cells. In sum, these findings demonstrate that distal nephron acidification pathways are dysregulated in KLHL3-KI mice. Whereas RHCG downregulation appears to be potassium-dependent, ATP6V1B1 reduction persists despite correction of hyperkalemia, suggesting the involvement of potassium-independent mechanisms. Our findings raise the possibility that dysregulated KLHL3 signaling contributes to impaired distal nephron acidification in type 4 RTA, which merits further investigation.
miR-1260b mediates rehabilitation of postpartum pelvic floor dysfunction by targeting PIN1.
Sun J, Yu C
Biochem Biophys Res Commun · 2026 Jun · PMID 42361742 · Publisher ↗
BACKGROUND: Postpartum pelvic floor dysfunction (PFD) impairs women's quality of life with unmet needs in early diagnosis and treatment. This study explored the expression profile, diagnostic value, and molecular mechani...
BACKGROUND: Postpartum pelvic floor dysfunction (PFD) impairs women's quality of life with unmet needs in early diagnosis and treatment. This study explored the expression profile, diagnostic value, and molecular mechanism of miR-1260b in postpartum PFD. METHODS: This study included 60 PFD cases and 60 healthy controls. The expression of miR-1260b in tissues was detected, and the diagnostic efficacy and risk factors were analyzed through receiver operating characteristic (ROC) and logistic regression. Pearson analysis was used to investigate the correlation between miR-1260b expression and bladder neck mobility (BNM) and levator ani hiatus area (ASHA). In vitro, human uterosacral ligament fibroblasts (hUSLFs) were treated with advanced glycation end products (AGEs). Functional assays (CCK-8, qRT-PCR, Western blot, dual-luciferase reporter assay) were performed after transfection with miR-1260b mimics/inhibitors or small interfering RNA to evaluate cell proliferation, oxidative stress, fibrosis, and signaling pathways, and validate target genes. RESULTS: miR-1260b was significantly upregulated in PFD tissues, showing positive correlations with BNM and ASHA (r = 0.774 and 0.741). It exhibited favorable diagnostic efficacy (AUC = 0.846) and served as an independent risk factor (OR = 9.671). AGE upregulated miR-1260b, suppressed hUSLF proliferation, enhanced oxidative stress and fibrosis, and altered extracellular matrix and FAK/RhoA pathway-related protein levels; these impairments were reversed by miR-1260b inhibition. PIN1 was identified as a direct target of miR-1260b, and PIN1 knockdown abrogated the protective effects of miR-1260b inhibitors. CONCLUSION: This study is the first to identify miR-1260b as a potential diagnostic biomarker for postpartum PFD, which mediates AGE-induced hUSLF dysfunction by targeting PIN1, providing novel targets for early diagnosis and targeted intervention.
Dual roles of JMJD6 in oncogenesis and immune evasion: molecular mechanisms and therapeutic prospects.
Chen SY, Zhang J, Yu XM … +3 more , Wang MN, Hao HX, Zheng Q
Biochem Biophys Res Commun · 2026 Jun · PMID 42361741 · Publisher ↗
JMJD6 is an iron (Fe)- and α-ketoglutarate (2-OG)-dependent dioxygenase that exhibits multiple enzymatic activities. As a key regulator of epigenetic and post-transcriptional processes, JMJD6 is frequently overexpressed...
JMJD6 is an iron (Fe)- and α-ketoglutarate (2-OG)-dependent dioxygenase that exhibits multiple enzymatic activities. As a key regulator of epigenetic and post-transcriptional processes, JMJD6 is frequently overexpressed in various malignancies and is closely associated with poor patient prognosis. This review systematically examines the central role of JMJD6 in tumorigenesis and cancer progression. Specifically, JMJD6 directly promotes tumor cell proliferation, invasion, metastasis, and stemness maintenance through mechanisms such as p53 hydroxylation and activation of the β-catenin/c-Myc signaling pathway. Furthermore, JMJD6 actively influences the immunosuppressive tumor microenvironment that facilitates tumor immune evasion, for example, by promoting M2-type tumor-associated macrophage polarization through the STAT3/IL-10 axis. Consequently, JMJD6 emerges as a multifunctional enzyme connecting intrinsic oncogenic programs with extrinsic immunosuppressive microenvironments. Given its pivotal roles, JMJD6 has become a promising prognostic biomarker and therapeutic target. Targeting JMJD6, particularly in combination with immune checkpoint inhibitors, represents a promising but still experimental strategy that warrants further investigation. This review further summarizes recent advances in JMJD6-targeted small-molecule inhibitors and combination therapy strategies, while discussing current challenges and future directions for clinical translation.
Non-fused ring A-D-A-type dyes for near-infrared II fluorescence imaging guided phototherapy and immune activation of tumour.
Wang J, Chen X, Tang Y … +5 more , Pang E, Xia D, Chen Y, He D, Wang K
Biochem Biophys Res Commun · 2026 Jun · PMID 42361740 · Publisher ↗
Phototherapy has gained considerable attention in cancer treatment. Molecules with pronounced near-infrared (NIR) absorption are particularly advantageous for laser-induced phototherapy, as their NIR absorption enables d...
Phototherapy has gained considerable attention in cancer treatment. Molecules with pronounced near-infrared (NIR) absorption are particularly advantageous for laser-induced phototherapy, as their NIR absorption enables deep tissue penetration while minimizing incidental damage to healthy tissues. In this study, we rationally designed and synthesized a non-fused ring A-D-A-type dye (T8IC4F) exhibiting both NIR absorption and fluorescence properties. Through self-assembly of T8IC4F with DSPE-PEG-NH, water-dispersible nanoparticles (NPs) designated as C4@PEG were fabricated. The resulting C4@PEG NPs exhibit NIR absorption and NIR-II fluorescence properties and demonstrate significant therapeutic efficacy. Upon 808 nm laser irradiation (1 W cm), these NPs exhibit a singlet oxygen (O) quantum yield of 25.9% and a photothermal conversion efficiency of 61%. These properties enable them to mediate both photodynamic and photothermal therapy, leading to robust antitumor efficacy. Moreover, C4@PEG NPs induce immunogenic cell death, facilitate the release of tumor antigens, and activate an antitumor immune response. These findings suggest that C4@PEG NPs could be applied in cancer phototherapy and immunotherapy.
DCAF13 is associated with pancreatic ductal adenocarcinoma progression and p53-related signaling in TP53-mutant cells.
Fan X, Zhao H, Wu B … +8 more , Lv Y, Chen W, Chen Q, Hu L, Yu S, Wang J, He Y, Yu J
Biochem Biophys Res Commun · 2026 Jun · PMID 42361739 · Publisher ↗
BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with poor prognosis. DDB1 and CUL4 associated factor 13 (DCAF13) has been implicated in tumor progression, but its clinical relevance...
BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with poor prognosis. DDB1 and CUL4 associated factor 13 (DCAF13) has been implicated in tumor progression, but its clinical relevance and biological function in PDAC remain unclear. METHODS: Public databases (GEPIA2 and Kaplan-Meier Plotter) were used to analyze DCAF13 expression and its prognostic value in PDAC. Tumor and paired adjacent tissues from 90 PDAC patients were examined by immunohistochemistry to assess DCAF13 protein expression and its association with clinicopathological features and survival. DCAF13 expression in HPDE6-C7, AsPC-1 and MiaPaCa-2 cells was detected by qRT-PCR and Western blotting. Gain- and loss-of-function models were established to evaluate the effects of DCAF13 on cell migration, invasion and apoptosis using wound healing, Transwell and flow cytometry assays. Changes in p53-related signaling proteins were examined by Western blot. RESULTS: Bioinformatic analyses revealed significantly elevated DCAF13 expression in PDAC and its association with shorter overall and disease-free survival. Clinically, DCAF13 protein was overexpressed in PDAC tissues and correlated with tumor differentiation (P = 0.006). In PDAC cell lines, DCAF13 knockdown suppressed migration and invasion while promoting apoptosis in vitro, whereas DCAF13 overexpression exerted the opposite effects. In TP53-mutant PDAC cells, DCAF13 knockdown was associated with increased expression of p53-related proteins, including p53 and its downstream targets p21, BAX and FAS, suggesting a potential association between DCAF13 and altered p53-related signaling in this cellular context. CONCLUSIONS: DCAF13 is overexpressed in PDAC and associated with poor prognosis. DCAF13 may promote malignant phenotypes in vitro and alter p53-related signaling in TP53-mutant PDAC cells. These findings suggest that DCAF13 may have potential value as a prognostic biomarker and exploratory therapeutic candidate for PDAC, although further validation in WT-p53 and in vivo models is still required.
Visualization and detection of ciliary beating frequency in human airway organoids based on image correlated methods for drug screening.
Sun R, Wang D, Gao C … +7 more , Bing Z, Du J, Zhang L, Wu T, Li Z, Liang N, Dong W
Biochem Biophys Res Commun · 2026 Jun · PMID 42361738 · Publisher ↗
Respiratory ciliary motion is critical for airway hygiene, as its directional beating clears pathogens and debris. Dysfunctional cilia lead to mucus buildup, infections, and worsened respiratory diseases. However, studyi...
Respiratory ciliary motion is critical for airway hygiene, as its directional beating clears pathogens and debris. Dysfunctional cilia lead to mucus buildup, infections, and worsened respiratory diseases. However, studying ciliary dynamics remains challenging due to technical limitations in imaging and analysis. To address this, human airway organoids expressing specific biomarkers were cultured, and ciliary motility was captured using a charge-coupled device camera. Wavelet transform-based image processing reduced background noise and enhanced cilia contours, enabling color visualization and automated motion analysis. An image-processing motion-tracking system was developed to quantify ciliary beating frequency (CBF), integrating optical stabilization, computational enhancement, and pattern recognition. This method provided spatiotemporal visualization, segmented frequency values, correlation coefficient curves, and dynamic analysis videos with real-time updates. Automated cilia recognition improved localization during movement, minimizing interference. Using this platform, Roflumilast and procaterol were identified as effective enhancers of ciliary beating. Transcriptomic analysis further revealed key regulatory networks governing ciliary structure and function. This framework combines mechanistic insights with therapeutic screening, offering a powerful tool for advancing respiratory research and clinical applications. By enabling precise, high-resolution ciliary motion analysis, this approach addresses longstanding challenges in the field and opens new avenues for targeted therapies in respiratory pathologies.
Oral L-Serine and D-Serine acutely suppress postprandial hyperglycemia through inhibition of intestinal glucose absorption in healthy mice.
Toda A, Mohri S, Ueda K … +4 more , Daido K, Fuchisawa D, Furuya F, Mukai E
Biochem Biophys Res Commun · 2026 Jun · PMID 42361737 · Publisher ↗
D-Serine (D-Ser), an enantiomer of L-Serine (L-Ser), has been reported to exert unique physiological effects distinct from those of L-Ser. Chronic oral administration of L-Ser has been reported to improve glucose toleran...
D-Serine (D-Ser), an enantiomer of L-Serine (L-Ser), has been reported to exert unique physiological effects distinct from those of L-Ser. Chronic oral administration of L-Ser has been reported to improve glucose tolerance in diabetic model mice. In this study, we compared the acute effects of oral administration of L-Ser and D-Ser on postprandial blood glucose regulation and the underlying mechanisms in healthy mice. Oral glucose tolerance tests were performed in C57BL/6J mice administered L-Ser or D-Ser (2.0 g/kg BW) simultaneously with glucose loading. Both L-Ser and D-Ser significantly suppressed postprandial hyperglycemia compared with the control group. However, neither L-Ser nor D-Ser significantly affected serum insulin levels after glucose loading or insulin sensitivity during insulin tolerance tests, suggesting that their glucose-lowering effects were independent of insulin secretion and insulin sensitivity. In addition, intraperitoneal glucose tolerance tests showed no significant changes in postprandial hyperglycemia after administration of either L-Ser or D-Ser. In intestinal glucose absorption assays using everted intestine, both L-Ser and D-Ser significantly suppressed glucose absorption. Furthermore, Western blotting analysis demonstrated that L-Ser reduced GLUT2 expression in the brush border membrane, whereas D-Ser reduced both SGLT1 and GLUT2 expression. These findings demonstrate that single oral administration of l-/D-Ser acutely suppresses postprandial hyperglycemia independently of insulin secretion and insulin sensitivity by inhibiting intestinal glucose absorption. In addition, the underlying mechanisms may differ between L-Ser and D-Ser, as reflected by their distinct effects on intestinal glucose transporters, suggesting stereospecific regulation of intestinal glucose metabolism.
Analysis of the effect of polyanionic phosphates on the solvent features of aqueous media.
Corrigan LE, Titus AR, Ferreira LA … +2 more , Uversky VN, Zaslavsky BY
Biochem Biophys Res Commun · 2026 Jun · PMID 42361736 · Publisher ↗
Adenosine triphosphate (ATP) has emerged as a critical regulator of liquid-liquid phase separation (LLPS), protein aggregation, and cytoplasmic fluidity, yet the molecular basis of its effects remains incompletely unders...
Adenosine triphosphate (ATP) has emerged as a critical regulator of liquid-liquid phase separation (LLPS), protein aggregation, and cytoplasmic fluidity, yet the molecular basis of its effects remains incompletely understood. In this study, attenuated total reflectance Fourier-transform infrared (ATR-FTIR) spectroscopy combined with Gaussian decomposition of the OH-stretch region was used to investigate the effects of ATP on hydrogen-bond organization in aqueous phosphate-buffered solutions. Four water subpopulations corresponding to distinct hydrogen-bond arrangements were analyzed to characterize ATP-induced restructuring of the solvent network. Increasing ATP concentrations produced a reproducible increase in the contribution of the strong tetrahedrally hydrogen-bonded water subpopulation (3080 cm), while the relative contributions of more weakly hydrogen-bonded water populations remained largely unchanged. Similar but stronger effects were observed for sodium triphosphate, whereas DNA and longer-chain polyphosphates did not exhibit comparable behavior. These findings suggest that ATP and related triphosphates modulate aqueous hydrogen-bond organization through selective stabilization of highly coordinated water structures rather than broad disruption of the hydrogen-bond network. The results provide new insight into solvent restructuring mechanisms that may contribute to ATP-mediated solubilization, condensate regulation, and cytoplasmic fluidization.
Retraction notice to "REGγ regulates ERα degradation via ubiquitin-proteasome pathway in breast cancer" [Biochem. Biophys. Res. Commun. 456 (2015) 534-540].
Chai F, Liang Y, Bi J … +4 more , Chen L, Zhang F, Cui Y, Jiang J
Biochem Biophys Res Commun · 2026 Aug · PMID 42350216 · Publisher ↗
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Astragaloside II-preconditioned bone marrow mesenchymal stem cells attenuate sepsis-induced acute lung injury by restoring mitochondrial function via NRF2/PGC-1α pathway activation.
Zhang H, Sun Y, Tang Y … +3 more , Yao L, Abulimiti X, Wu Q
Biochem Biophys Res Commun · 2026 Jun · PMID 42349124 · Publisher ↗
OBJECTIVE: Sepsis-induced acute lung injury (ALI) is characterized by mitochondrial dysfunction and oxidative stress, contributing to high mortality rates. This study investigates the protective effects of astragaloside...
OBJECTIVE: Sepsis-induced acute lung injury (ALI) is characterized by mitochondrial dysfunction and oxidative stress, contributing to high mortality rates. This study investigates the protective effects of astragaloside II (ASII)-preconditioned bone marrow mesenchymal stem cells (BMSCs) on sepsis-induced ALI and explores the underlying mechanism. METHODS: BMSCs were isolated from C57BL/6 mice and preconditioned with ASII. The viability, migration, and apoptosis of these BMSCs were assessed. LPS-injured MLE-12 cells were co-cultured with ASII-preconditioned BMSCs to evaluate their protective effects on cell survival, apoptosis, mitochondrial membrane potential, and oxidative stress markers. A cecal ligation and puncture (CLP)-induced sepsis model in mice was used to assess the in vivo efficacy of ASII-preconditioned BMSCs on lung injury, pulmonary edema, inflammation, and apoptosis. The involvement of the NRF2 pathway was confirmed using a specific inhibitor, ML385. RESULTS: BMSCs pretreated with ASII exhibited enhanced viability, migration, and resistance to apoptosis. In LPS-injured MLE-12 cells, ASII-preconditioned BMSCs improved cell survival, reduced apoptosis, and restored mitochondrial membrane potential by modulating mitochondrial dynamics (increasing Mfn2 and decreasing Fis1 expression) and promoting mitochondrial biogenesis via the NRF2/PGC-1α/Nrf1/Tfam signaling axis. These protective effects were attenuated upon NRF2 inhibition with ML385, confirming NRF2 pathway involvement. In a CLP-induced sepsis model, ASII-preconditioned BMSCs significantly reduced lung injury, pulmonary edema, and apoptosis, while lowering inflammatory cytokine levels (TNF-α, IL-1β, IL-6) and increasing TIPE2 in bronchoalveolar lavage fluid. CONCLUSIONS: Collectively, these findings highlight ASII preconditioning as an effective strategy to enhance BMSCs therapeutic efficacy for sepsis-induced ALI through NRF2-mediated mitochondrial protection.
Identification of an isoquinoline-derived quinazoline hybrid as a transcriptional inhibitor of fatty acid synthase to suppress hepatitis C virus production.
Wang X, Satoh S, Jiao M … +6 more , Konno A, Ito M, Sato A, Kadofusa N, Iwatani Y, Suzuki T
Biochem Biophys Res Commun · 2026 Jun · PMID 42349123 · Publisher ↗
Host-directed antiviral strategies provide an alternative approach to overcome the rapid emergence of drug-resistant viruses. Fatty acid synthase (FASN), a key enzyme in de novo lipogenesis, is exploited by multiple viru...
Host-directed antiviral strategies provide an alternative approach to overcome the rapid emergence of drug-resistant viruses. Fatty acid synthase (FASN), a key enzyme in de novo lipogenesis, is exploited by multiple viruses to support their life cycles. To date, FASN-targeted therapies have focused on enzyme activity inhibition. However, since catalytic inhibition of FASN carries the risk of disrupting lipid homeostasis in normal tissues, FASN expression suppression was considered a potentially effective alternative. To identify inhibitors of FASN expression, we established a CRISPR-engineered HuH-7 reporter cell line in which a HiBiT tag was knocked into the endogenous FASN locus, enabling quantitative monitoring of native FASN protein levels. The high-throughput screening of 19,912 small molecules resulted in the identification of a potent suppressor of FASN production: an isoquinoline-derived quinazoline hybrid designated IQZ-1. Promoter analyses revealed that IQZ-1 inhibits FASN transcription at least via the proximal sterol regulatory elements of the FASN promoter. Using hepatitis C virus (HCV) as a lipid-dependent model virus, we demonstrated that IQZ-1 significantly reduced intracellular viral RNA levels and markedly suppressed infectious particle production. Subgenomic replicon analyses indicated partial inhibition of viral genome replication, while immunofluorescence studies revealed reduced abundance of lipid droplets, essential platforms for HCV virion formation, in infected cells. These findings suggest that transcriptional suppression of FASN impairs both membrane-associated replication complex formation and virion assembly. Collectively, our results establish proof of concept that targeting FASN synthesis, rather than enzymatic activity, effectively disrupts lipid-dependent viral propagation and represents a promising host-directed antiviral strategy.
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