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18611424007
Signal Transduction and
Targeted Therapy [IF=40.8]
文獻引用產(chǎn)品：
bs-0201R | GDNFRA Rabbit pAb | IHC
作者單位：中國醫(yī)科大學盛京醫(yī)院
摘要：Significant heterogeneity exists in hormone receptor(HR)-positive/HER2-positive(HR+/HER2+) breast cancer, contributing to suboptimal pathological complete response rates with conventional neoadjuvant treatment regimens. Overcoming this challenge requires precise molecular classification, which is pivotal for the development of targeted therapies. We conducted molecular typing on a cohort of 211 patients with HR+/HER2+ breast cancer and performed a comprehensive analysis of the efficacy of various neoadjuvant treatment regimens. Our findings revealed four distinct molecular subtypes, each exhibiting unique characteristics and therapeutic implications. The HER2-enriched subtype, marked by activation of the HER2 signaling and hypoxia-inducible factor 1(HIF-1) pathway, may benefit from intensified anti-HER2-targeted therapy. Estrogen receptor(ER)-activated subtype demonstrated potential sensitivity to combined therapeutic strategies targeting both ER and HER2 pathways. Characterized by high immune cell infiltration, the immunomodulatory subtype showed sensitivity to HER2-targeted antibody–drug conjugates(ADCs) and promise for immune checkpoint therapy. The highly heterogeneous subtype requires a multifaceted therapeutic approach. Organoid susceptibility assays suggested phosphoinositide 3-kinase inhibitors may be a potential treatment option. These findings underscore the importance of molecular subtyping in HR+/HER2+ breast cancer, offering a framework for developing precise and personalized treatment strategies. By addressing the heterogeneity of the disease, these approaches have the potential to optimize therapeutic outcomes and improve patient care.
dvanced Materials [IF=28.7]
文獻引用產(chǎn)品：
bs-0295G-BF488 | Goat Anti-Rabbit IgG H&L, BF488 conjugated | IF
作者單位：南京醫(yī)科大學第一附屬醫(yī)院
Engineering [IF=27.7]
文獻引用產(chǎn)品：
bs-0647R | CD4 Rabbit pAb | IHC
作者單位：中國科學技術(shù)大學附屬第一醫(yī)院
摘要：Tolerogenic antigen-presenting cells(APCs) are promising as therapeutics for suppressing T cell activation in autoimmune diseases. However, the isolation and ex vivo manipulation of autologous APCs is costly, and the process is customized for each patient. Here we show that tolerogenic APCs can be generated in vivo by delivering, via lipid nanoparticles, messenger RNA coding for the inhibitory protein programmed death ligand 1. We optimized a lipid-nanoparticle formulation to minimize its immunogenicity by reducing the molar ratio of nitrogen atoms on the ionizable lipid and the phosphate groups on the encapsulated mRNA. In mouse models of rheumatoid arthritis and ulcerative colitis, subcutaneous delivery of nanoparticles encapsulating mRNA encoding programmed death ligand 1 reduced the fraction of activated T cells, promoted the induction of regulatory T cells and effectively prevented disease progression. The method may allow for the engineering of APCs that target specific autoantigens or that integrate additional inhibitory molecules.
Nature Neuroscience [IF=21.3]
文獻引用產(chǎn)品：
摘要：Astrocytes promote neuroinflammation and neurodegeneration in multiple sclerosis(MS) through cell-intrinsic activities and their ability to recruit and activate other cell types. In a genome-wide CRISPR-based forward genetic screen investigating regulators of astrocyte proinflammatory responses, we identified the C-type lectin domain-containing 16A gene(CLEC16A), linked to MS susceptibility, as a suppressor of nuclear factor-κB (NF-κB) signaling. Gene and small-molecule perturbation studies in mouse primary and human embryonic stem cell-derived astrocytes in combination with multiomic analyses established that CLEC16A promotes mitophagy, limiting mitochondrial dysfunction and the accumulation of mitochondrial products that activate NF-κB, the NLRP3 inflammasome and gasdermin D. Astrocyte-specific Clec16a inactivation increased NF-κB, NLRP3 and gasdermin D activation in vivo, worsening experimental autoimmune encephalomyelitis, a mouse model of MS. Moreover, we detected disrupted mitophagic capacity and gasdermin D activation in astrocytes in samples from individuals with MS. These findings identify CLEC16A as a suppressor of astrocyte pathological responses and a candidate therapeutic target in MS.
Bioactive Materials [IF=18]
文獻引用產(chǎn)品：
摘要：Osteochondral autograft transfer system(OATS) can effectively improve cartilage injuries by obtaining bone-cartilage grafts from healthy sites and implanting them into the defective areas. However, in up to 40% of patients, the lack of a stable adhesive interface between the osteochondral graft and the normal tissue surface reduces the repair efficiency. In this work, we report an injectable and biocompatible poly(N-hydroxyethyl acrylamide-N-hydroxy succinimide)/Gelatin (PHE-Gel) hydrogel, featuring the instant formation of a tough bio-interface, which allows for robust adhesion with osteochondral grafts. Through physicochemical characterization, we found that a system composed of 10%PHE-Gel possesses superior interfacial toughness and excellent biocompatibility. In vitro, mechanistic studies and RNA-seq analysis had shown that 10%PHE-Gel promotes the expression of cartilage anabolic metabolism genes by upregulating the hypoxia-inducible factor alpha (HIF-α) signaling pathway and downregulating the tumor necrosis factor(TNF) signaling pathway. Dimethyloxalylglycine(DMOG) loaded liposome (DMOG-Lip) promotes the transition of M1 macrophages to M2 macrophages, shifting the microenvironment towards a pro-repair direction. Studies on a rabbit OATS model indicated that DMOG-Lip loaded 10%PHE-Gel(10%PHE-Gel@DMOG-Lip) effectively modulated the immune microenvironment, facilitated the repair of the hyaline cartilage, and inhibited further degeneration of cartilage. This composite hydrogel offers a promising solution for enhancing OATS repair in tissue engineering and has the potential to improve outcomes in cartilage restoration procedures.
Nucleic Acids Research [IF=16.7]
文獻引用產(chǎn)品：
作者單位：日本東北大學
摘要：The SWI/SNF chromatin-remodeling complex that comprises multiple subunits orchestrates diverse cellular processes, including gene expression, DNA repair, and DNA replication, by sliding and releasing nucleosomes. AT-interacting domain-rich protein 1A(ARID1A) and ARID1B (ARID1A/B), a pivotal subunit, have significant relevance in cancer management because they are frequently mutated in a broad range of cancer types. To delineate the protein network involving ARID1A/B, we investigated the interactions of this with other proteins under physiological conditions. The ARID domain of ARID1A/B interacts with proteins involved in transcription and DNA/RNA metabolism. Several proteins are responsible for genome integrity maintenance, including DNA-dependent protein kinase catalytic subunit(DNA-PKcs), bound to the armadillo(ARM) domain of ARID1A/B. Introducing a knock-in mutation at the binding amino acid of DNA-PKcs in HCT116 cells reduced the autophosphorylation of DNA-PKcs and the recruitment of LIG4 in response to ionizing radiation. Our findings suggest that within the SWI/SNF complex, ARID1A couples DNA double-strand break repair processes with chromatin remodeling via the ARM domains to directly engage with DNA-PKcs to maintain genome stability.
ACS Nano [IF=15.8]
文獻引用產(chǎn)品：
bs-0805R | CD56 Rabbit pAb | Other
摘要：Single-molecule tracking offers nanometer resolution for studying individual molecule dynamics but is often limited by sparse labeling to avoid signal overlap. We present Red-Light-Activated Single-molecule Tracking(RE-LAST) strategy to address this challenge utilizing a photoactivatable probe, SiR670. SiR670 combines traditional silicon rhodamine with a photocage called SO, quenching fluorescence via photoinduced electron transfer(PET). Red light triggers SiR670 excitation, generating singlet oxygen that oxidizes the SO cage, halting PET and restoring fluorescence. RE-LAST used red light for both activation and imaging, eliminating harmful UV exposure. This method enables high-throughput single-molecule tracking, achieving approximately 9 times more tracks than conventional methods and allowing detailed classification of CD56 membrane protein motion. Furthermore, in situ imaging of single live cells revealed the effects of triplet quencher and oxygen scavenging system(OSS) on membrane protein dynamics. While triplet quenchers like Trolox had minimal impact on protein movement patterns, OSS significantly accelerated protein movement and increased the proportion of mobile proteins. This approach provides a comprehensive method for investigating membrane protein dynamics in living cells, contributing to further developments in cellular and molecular biology.
ACS Nano [IF=15.8]
文獻引用產(chǎn)品：
作者單位：捷克科學院
摘要：Lead nanoparticles(PbNPs) in air pollution pose a significant threat to human health, especially due to their neurotoxic effects. In this study, we exposed mice to lead(II) oxide nanoparticles(PbONPs) in inhalation chambers to mimic real-life exposure and assess their impact on the brain. PbONPs caused the formation of Hirano bodies and pathological changes related to neurodegenerative disorders through cytoskeletal disruptions without the induction of inflammation. Damage to astrocytic endfeet and capillary endothelial cells indicated a compromised blood–brain barrier(BBB), allowing PbONPs to enter the brain. Additionally, NPs were detected along the olfactory pathway, including fila olfactoria, suggesting that at least a proportion of PbNPs enter the brain directly by passing through the olfactory epithelium. PbNP inhalation severely damaged the apical parts of olfactory epithelial cells, including the loss of microtubules in their ciliary distal segments. Inhalation of PbONPs led to the rapid accumulation of lead in the brain, while more soluble lead(II) nitrate NPs did not accumulate significantly until 11 weeks of exposure. PbNPs induced disruption of the BBB at multiple levels, ranging from ultrastructural changes to functional impairments of the barrier; however, they did not induce systemic inflammation in the brain. The clearance ability of the brain to remove Pb was very low for both types of NPs, with significant pathological effects persisting even after a long clearance period. Cation-binding proteins(ZBTB20 and calbindin1) were distributed unevenly in the brain, with the strongest signal located in the hippocampus, which exhibited the greatest defects in nuclear architecture, indicating that this area is the most sensitive structure for PbNP exposure. PbNP exposure also altered the PI3K/Akt/mTOR signaling pathway, and tau phosphorylation in the hippocampus and inhibition of tau phosphorylation by GSK-3 inhibitor rescued the negative effect of PbONPs on the intracellular calcium level in trigeminal ganglion cultures. In zebrafish larvae, PbONPs affected locomotor activity and reduced calcium levels in the medium enhanced negative effect of PbONP on animal mobility, even increasing lethality. These findings suggest that cytoskeletal disruption and calcium dysregulation are key factors in PbNP-induced neurotoxicity, providing potential targets for therapeutic intervention to prevent neurodegenerative changes following PbNP exposure.
ACS Nano [IF=15.8]
文獻引用產(chǎn)品：
bs-1441R | CXCL16 Rabbit pAb | IF
bs-2454R | CCL19 Rabbit pAb | IF
作者單位：中國科學技術(shù)大學第一附屬醫(yī)院
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