Biochemical and biophysical research communications最新文献

{"title":"A single amino acid substitution increases both carboxylation turnover number and CO2 affinity of form II Rubisco","authors":"Junli Zhang ,&nbsp;Lei Zhao ,&nbsp;Guoxia Liu ,&nbsp;Yanping Zhang ,&nbsp;Zhen Cai ,&nbsp;Yin Li","doi":"10.1016/j.bbrc.2025.151940","DOIUrl":"10.1016/j.bbrc.2025.151940","url":null,"abstract":"<div><div>Ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco), the key CO₂-fixing enzyme in photosynthesis, is notorious for its low carboxylation activity. However, the difficulty in rationally engineering a fast Rubisco over the past decades brings a question whether a constraint exists in Rubisco's catalytic mechanism. In this study, we show that altering a single amino acid at position 398 in Form II Rubisco doubles its catalytic efficiency. The T398S and T398A mutations of the Form II Rubisco from the symbiont of <em>Riftia pachyptila</em> increases activity by 61 % and 74 %, respectively. The T398A mutant exhibits a turnover number (<em>k</em>_cat^C) of 35.84 s⁻¹, twice that of the wild type. Structural simulation analysis indicates that the distance between the amino acid residues at position 398 and 395 influences weak hydrogen bond formation. Remarkably, these enhancements were achieved without compromising CO₂ affinity (<em>K</em>_M^C), challenging the conventional trade-off paradigm. Our findings not only identify residue 398 as a critical determinant of Rubisco's performance but also highlight the untapped potential for engineering more efficient CO₂-fixing enzymes.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"768 ","pages":"Article 151940"},"PeriodicalIF":2.5,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PEX5 acts as a negative regulator of RANKL-induced osteoclastogenesis in vitro and inflammatory calvarial bone destruction in vivo","authors":"So Young Eun ,&nbsp;Yoon-Hee Cheon ,&nbsp;Chang Hoon Lee ,&nbsp;Chong Hyuk Chung ,&nbsp;Myeung Su Lee ,&nbsp;Ju-Young Kim","doi":"10.1016/j.bbrc.2025.151924","DOIUrl":"10.1016/j.bbrc.2025.151924","url":null,"abstract":"<div><div>Peroxisomal biogenesis factor 5 (PEX5), a peroxisomal import receptor, is well recognized for its role in protein trafficking and oxidative stress regulation. However, its function in bone metabolism remains unclear. Given the established impact of oxidative stress on osteoclast differentiation, this study explores the previously uncharacterized role of PEX5 in osteoclastogenesis and bone resorption. Using bone marrow-derived macrophages, we examined the effects of PEX5 knockdown (siPEX5) and recombinant PEX5 protein (rpPEX5) on osteoclast differentiation. Osteoclast activity was evaluated through TRAP staining, F-actin ring formation, and bone resorption assays. qRT-PCR and Western blot analyses assessed gene and protein expression, while an lipopolysaccharide (LPS)-induced calvarial bone loss model provided <em>in vivo</em> validation. PEX5 expression declined during osteoclast differentiation, and its suppression promoted osteoclastogenesis by increasing c-Fos, NFATc1, and osteoclast-specific gene expression. Loss of PEX5 also enhanced receptor activator of nuclear factor kappa-Β ligand (RANKL)-induced activation of Akt, MAPK, IκB, and calcium-dependent pathways, accelerating osteoclast maturation. In contrast, rpPEX5 treatment effectively inhibited osteoclast differentiation and bone resorption by downregulating NFATc1 and dampening RANKL-mediated signaling. <em>In vivo</em>, rpPEX5 administration mitigated LPS-induced bone loss by preserving bone structure and reducing osteoclast activity. These findings reveal a novel function of PEX5 as a regulator of osteoclast differentiation, independent of its peroxisomal role. The extracellular activity of PEX5 suggests a broader regulatory mechanism in bone metabolism, with potential therapeutic implications for osteolytic diseases.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"767 ","pages":"Article 151924"},"PeriodicalIF":2.5,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143899498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Berberine alleviates tendinopathy by suppressing the cGAS-STING pathway and Relieving ferroptosis","authors":"Yeshuai Shen ,&nbsp;Wenting Wei ,&nbsp;Yang Lu ,&nbsp;Mingyuan Song ,&nbsp;Shaojie Yang ,&nbsp;Huan Liu ,&nbsp;Xingquan Xu ,&nbsp;Haibin Zhou","doi":"10.1016/j.bbrc.2025.151923","DOIUrl":"10.1016/j.bbrc.2025.151923","url":null,"abstract":"<div><div>Berberine, a key bioactive component of Coptis rhizome, has been extensively studied for its therapeutic effects on various diseases. This research aimed to investigate the potential benefits of berberine in treating tendinopathy and to elucidate the underlying mechanisms through animal and laboratory studies. Our findings indicated that berberine effectively treated type I collagenase-induced tendinopathy in rats, confirmed by cellular-level validation. At the molecular level, berberine reduced the activation of the cGAS-STING signaling pathway and decreased the accumulation of malondialdehyde (MDA) and reactive oxygen species (ROS) in both animal models and cell cultures. Additionally, berberine upregulated the expression of glutathione (GSH) and glutathione peroxidase 4 (GPX4) in tissues. These results suggested that berberine alleviated ferroptosis via the cGAS-STING pathway, thus exerting therapeutic effects on tendinopathy. To validate these findings further, we administered the ferroptosis inducer Imidazole Ketone Erastin (IKE) to evaluate the effects of berberine. IKE significantly diminished the therapeutic effects of berberine on tendinopathy, as indicated by the previously mentioned markers. Thus, berberine mitigated ferroptosis by inhibiting the cGAS-STING pathway, highlighting its potential in managing tendinopathy.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"767 ","pages":"Article 151923"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143899496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Key thermodynamic characteristics of Cas9 and Cas12a endonucleases’ cleavage of a DNA substrate containing a nucleotide mismatch in the region complementary to RNA","authors":"Svetlana V. Baranova ,&nbsp;Polina V. Zhdanova ,&nbsp;Pavel E. Pestryakov ,&nbsp;Alexander A. Chernonosov ,&nbsp;Vladimir V. Koval","doi":"10.1016/j.bbrc.2025.151892","DOIUrl":"10.1016/j.bbrc.2025.151892","url":null,"abstract":"<div><div>CRISPR-Cas9 and CRISPR-Cas12a are endonuclease systems widely used for genome editing, but their mechanisms of DNA cleavage, particularly in the presence of nucleotide mismatches, remain incompletely understood. This study deals with thermodynamic parameters governing the cleavage of DNA substrates—containing a mismatch in the region complementary to RNA—by Cas9 and Cas12a. Using a series of 55 bp DNA substrates with various mismatches, we investigated the cleavage efficiency, reaction kinetics, and thermodynamic stability of the Cas12a–crRNA complex and compared it with Cas9–sgRNA on the same substrates. Cas12a manifested strict specificity, with a mismatch leading to a significant reduction in cleavage efficiency or to nonspecific <em>trans</em>-cleavage, whereas Cas9 showed higher tolerance to each mismatch, especially in internal and distal regions. Thermodynamic calculations indicated that Cas12a–crRNA complexes are generally stabler with fully complementary DNA but are more destabilized by a mismatch than Cas9–sgRNA complexes are. Molecular dynamics simulations revealed that a mismatch causes greater structural destabilization in Cas12a than in Cas9, correlating with reduced cleavage efficiency. These findings highlight distinct mechanisms of mismatch recognition by Cas9 and Cas12a, provide insights into their enzymatic behavior, and inform the design of more precise genome-editing tools.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"768 ","pages":"Article 151892"},"PeriodicalIF":2.5,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"It takes Two: Advancing cancer treatment with two-step nanoparticle delivery","authors":"Elena N. Komedchikova,&nbsp;Olga A. Kolesnikova,&nbsp;Anastasiia S. Obozina,&nbsp;Arina O. Antonova,&nbsp;Alexei M. Dukat,&nbsp;Polina A. Fedotova,&nbsp;Daria S. Khardikova,&nbsp;Daniil V. Sokol,&nbsp;Iana O. Shimanskaia,&nbsp;Anna V. Svetlakova,&nbsp;Victoria O. Shipunova","doi":"10.1016/j.bbrc.2025.151921","DOIUrl":"10.1016/j.bbrc.2025.151921","url":null,"abstract":"<div><div>The rapid advancement of nanobiotechnology has resulted in the development of numerous targeted nanoformulations and sophisticated nanobiorobots for biomedical applications. Despite the potential of nanostructures to improve drug delivery and therapeutic efficacy, their clinical application is still constrained by insufficient accumulation in tumor tissues. Current methodologies result in only an average of 0.6 % of administered nanoparticles reaching tumors, prompting the development of innovative strategies to improve targeting and influence the pharmacokinetics and pharmacodynamics of drugs. One such approach is two-step targeting, which includes either the concept of tumor pre-targeting with specific recognizing elements or the stimuli-sensitive activation of nanostructures. This review critically evaluates advancements in two-step drug delivery systems utilizing nanobiotechnology for targeted cancer therapy. For instance, two-step delivery based on the pre-targeting concept involves an initial injection of targeting molecules that bind to tumor-specific antigens, followed by the administration of drug-loaded nanocarriers modified with complementary adaptors. This approach enhances nanoparticle accumulation in tumors and improves therapeutic outcomes by increasing interaction avidity and overcoming steric hindrances. We critically assess existing adaptor systems for two-step drug delivery and synthesize findings from various studies demonstrating their efficacy in both <em>in vitro</em> and <em>in vivo</em> settings, while addressing challenges in clinical translation. We also explore future directions for developing novel adaptor systems to enhance two-step delivery mechanisms. This review aims to contribute to optimizing nanobiotechnology in oncology for more effective cancer therapies.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"767 ","pages":"Article 151921"},"PeriodicalIF":2.5,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143896026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomes derived from human umbilical cord mesenchymal stem cells can reverse ventricular remodeling and improve long-term cardiac function after acute myocardial infarction","authors":"Renjie Wang ,&nbsp;Lulu Liu ,&nbsp;Fusheng Han,&nbsp;Qian Ma,&nbsp;Hua He","doi":"10.1016/j.bbrc.2025.151920","DOIUrl":"10.1016/j.bbrc.2025.151920","url":null,"abstract":"<div><h3>Background</h3><div>Acute myocardial infarction (AMI) is the most common ischemic heart disease with high morbidity and high mortality. Although the treatment of AMI is constantly developing, ischemia-reperfusion (I/R) injury remains a complex problem. In recent years, human umbilical cord-derived mesenchymal stem cell-derived exosomes (hUC-MSC-EXO) have been shown to alleviate related damages. However, the long-term effects, safety, and mechanism of action have not yet been fully explored.</div></div><div><h3>Methods</h3><div>We constructed human umbilical cord-derived mesenchymal stem cell-derived engineered exosomes. We compared the short-term and long-term protective abilities of engineered exosomes on myocardium during I/R in cardiomyocytes and rat models, and determined their long-term safety. At the same time, key pathways and genes were predicted through exosome sequencing.</div></div><div><h3>Results</h3><div>hUC-MSC-EXO significantly reduced apoptosis, oxidative stress, and inflammation in both in vitro and in vivo models. In I/R rats, IMTP-EXO demonstrated superior cardioprotective effects, reducing myocardial fibrosis and improving left ventricular function compared to controls. Long-term studies showed enhanced ejection fraction (EF) and fractional shortening (FS) and reduced left ventricular end-diastolic dimensions (LVEDD). Fluorescence imaging revealed higher exosome accumulation in ischemic hearts. Genes related to cardiovascular diseases were obtained through cross-comparison of multiple databases. GO analysis revealed that protein binding was the most highly enriched term. KEGG analysis showed that these genes were primarily involved in apoptosis and the PI3K-Akt signaling pathways. The PPI network showed that TP53, TLR4, EGFR, MAPK3, and GJA1 are central genes of heart I/R injury. GJA1, HMGB1, and PTEN are considered to be key genes by comparing to the comparative toxicogenomic database (CTD).</div></div><div><h3>Conclusions</h3><div>This study demonstrates that hUC-MSC-derived exosomes, especially IMTP-EXO, are safe, feasible, and effective for reversing ventricular remodeling and improving cardiac function in rat MI models. GJA1, HMGB1, and PTEN may be the key genes associated with myocardial I/R injury. These findings provide critical insights for translating hUC-MSC-EXO into clinical applications for treating myocardial I/R injuries.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"768 ","pages":"Article 151920"},"PeriodicalIF":2.5,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143904032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-resolution structure reveals enhanced 14-3-3 binding by a mutant SARS-CoV-2 nucleoprotein variant with improved replicative fitness","authors":"Kristina V. Perfilova ,&nbsp;Ilya O. Matyuta ,&nbsp;Mikhail E. Minyaev ,&nbsp;Konstantin M. Boyko ,&nbsp;Richard B. Cooley ,&nbsp;Nikolai N. Sluchanko","doi":"10.1016/j.bbrc.2025.151915","DOIUrl":"10.1016/j.bbrc.2025.151915","url":null,"abstract":"<div><div>Replication of many viruses depends on phosphorylation of viral proteins by host protein kinases and subsequent recruitment of host protein partners. The nucleoprotein (N) of SARS-CoV-2 is heavily phosphorylated and recruits human phosphopeptide-binding 14-3-3 proteins early in infection, which is reversed prior to nucleocapsid assembly in new virions. Among the multiple phosphosites of N, which are particularly dense in the serine/arginine-rich interdomain region, phospho-Thr205 is highly relevant for 14-3-3 recruitment by SARS-CoV-2 N. The context of this site is mutated in most SARS-CoV-2 variants of concern. Among mutations that increase infectious virus titers, the S202R mutation (B.1.526 Iota) causes a striking replication boost (∼166-fold), although its molecular consequences have remained unclear. Here, we show that the S202R-mutated N phosphopeptide exhibits a 5-fold higher affinity for human 14-3-3ζ than the Wuhan variant and we rationalize this effect by solving a high-resolution crystal structure of the complex. The structure revealed an enhanced 14-3-3/N interface contributed by the Arg202 side chain that, in contrast to Ser202, formed multiple stabilizing contacts with 14-3-3, including water-mediated H-bonds and guanidinium pi-pi stacking. These findings provide a compelling link between the replicative fitness of SARS-CoV-2 and the N protein's affinity for host 14-3-3 proteins.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"767 ","pages":"Article 151915"},"PeriodicalIF":2.5,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143896024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quercetin protects red blood cells from aggregation, eryptosis, and delayed hemolysis caused by cell-free histones through sialic acid interaction","authors":"Kurnegala Manikanta ,&nbsp;Somanathapura K. NaveenKumar ,&nbsp;Shanmuga S. Mahalingam ,&nbsp;Vaddaragudisalu D. Sandesha ,&nbsp;Chandrashekar Tejas ,&nbsp;Mysuru L. Sumedini ,&nbsp;Kabburahalli Sunitha ,&nbsp;Kempaiah Kemparaju ,&nbsp;Kesturu S. Girish","doi":"10.1016/j.bbrc.2025.151859","DOIUrl":"10.1016/j.bbrc.2025.151859","url":null,"abstract":"<div><div>Histones are nuclear proteins and play a vital role in regulating gene expression. Cell free histones in the circulation proved as damage-associated molecular patterns and were positively associated with various inflammatory disease conditions. Also, cell-free histones directly induce toxicity toward blood cells and are implicated in vascular dysfunction. However, cell-free histones are known to induce RBCs dysfunction in several histone-associated disorders, leading to hypoxia conditions. In this study, we aimed to understand the mechanism underlying the dysfunction of RBCs induced by histones and explore the protective effect of quercetin. Histone treatment at lower doses induces RBCs aggregation while at higher doses it induces eryptosis and delayed hemolysis. Surprisingly, the removal of negatively charged sialic acid on the RBC membrane prevents histone-induced toxicity, thereby confirming the significance of the interaction between sialic acid and histone. Quercetin (QUE), a flavonoid, significantly inhibits histone-induced RBCs aggregation, eryptosis, and hemolysis. Most importantly, inhibition against the pro-coagulant phenotype of RBCs induced by histones, emphasizes the therapeutic potential of QUE on blood coagulation. Further, spectral and molecular docking studies confirm the interaction between histones and QUE. Collectively, this study highlights the therapeutic value of QUE in protecting the RBCs functions during histones-associated pathological conditions.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"767 ","pages":"Article 151859"},"PeriodicalIF":2.5,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143899497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Malyngamide C a potential inhibitor of protein synthesis Machinery targeting peptide deformylase enzyme","authors":"Swagat Ranjan Maharana ,&nbsp;Kiran Mahapatra ,&nbsp;Showkat Ahmad Mir ,&nbsp;Vishwajeet Mukherjee ,&nbsp;Binata Nayak","doi":"10.1016/j.bbrc.2025.151910","DOIUrl":"10.1016/j.bbrc.2025.151910","url":null,"abstract":"<div><div>Due to the rising incidence of antibiotic-resistant and bacterial illnesses, new therapeutic drugs are essential to target vital bacterial enzymes. Peptide deformylase is an attractive antibacterial target because it plays a pivotal role in protein synthesis. The present study was guided to identify the potential inhibitors of peptide deformylase (PDF), viz., computational methods such as molecular docking, molecular dynamics (MD) simulations, thermodynamic stability, free energy calculations, and ADMET analysis.</div><div>Here we observed the toxicity profile and drug-likeness of the in-house cyanopeptides database. The malyngamide C showed good oral bioavailability. Molecular docking experiments revealed that malyngamide C showed a better binding affinity of −8.81 kcal/mol than reference actinonin −7.08 kcal/mol. Next, MD simulations revealed that malyngamide C, tumonoic acid A, borophycin, and actinonin were found stable in the binding pocket of PDF observed for 300 ns. The binding posture was well-retained, with negligible RMSD, and found within permissible limits observed throughout the simulations. From the MM/PBSA calculations, the free binding energy of malyngamide C was found to be −145.281 kJ/mol, significantly exceeding other selected molecules, including actinonin. The malyngamide C could be a lead antibacterial candidate with a good safety profile. These computational findings strongly support its experimental validation and further clinical investigations as a novel antibacterial agent to combat drug-resistant bacterial infections.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"767 ","pages":"Article 151910"},"PeriodicalIF":2.5,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143899495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of CXCR4/SDF1 signaling in the initial migration of cardiac neural crest cells","authors":"Saori Tani-Matsuhana,&nbsp;Yumi Unozu,&nbsp;Kunio Inoue","doi":"10.1016/j.bbrc.2025.151914","DOIUrl":"10.1016/j.bbrc.2025.151914","url":null,"abstract":"<div><div>Neural crest cells are migratory and multipotent cell populations that give rise to various derivatives during the development of vertebrate embryos. The cells are specified in the neural folds and undergo epithelial mesenchymal transition (EMT) to delaminate and then migrate within the embryo. Cardiac neural crest cells originate from the caudal hindbrain and migrate through the pharyngeal arches to the heart. It has been shown that CXCR4/SDF1 signaling control cardiac neural crest cells migration toward pharyngeal arches in chicken embryos. Here, we investigated the effect of disruption of CXCR4/SDF1 signaling on cardiac neural crest cell migration by implanting beads into the lumen of the closing neural tube. We first observed that a CXCR4 antagonist inhibited initial cardiac neural crest migration. We also found that an ectopic source of SDF1 caused the accumulation of cardiac neural crest cells in the dorsal neural tube and the invasion of cardiac neural crest cells into the neural tube. Furthermore, disruption of signaling led to disorganization of the neural tube basement membrane but did not affect neural crest EMT. Overall, our data indicate that CXCR4/SDF1 signaling is critical for as early as the onset of cardiac neural crest cell migration after the delamination.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"767 ","pages":"Article 151914"},"PeriodicalIF":2.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143899551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}