源葉SCI文獻(xiàn)引用資訊 

 

1、CELL RESEARCH（IF=44.1)

文獻(xiàn)引用產(chǎn)品：

 

 

 

 

 

 

 

 

 

 

 

 

貨號	產(chǎn)品名稱	規(guī)格
R20497	多聚甲醛溶液	4% PFA

 

 

 

 

 

 

摘要：Here, we present a gene regulation strategy enabling programmable control over eukaryotic translational initiation. By excising the natural poly-adenylation (poly-A) signal of target genes and replacing it with a synthetic control region harboring RNA-binding protein (RBP)-specific aptamers, cap-dependent translation is rendered exclusively dependent on synthetic translation initiation factors (STIFs) containing different RBPs engineered to conditionally associate with different eIF4F-binding proteins (eIFBPs). This modular design framework facilitates the engineering of various gene switches and intracellular sensors responding to many user-defined trigger signals of interest, demonstrating tightly controlled, rapid and reversible regulation of transgene expression in mammalian cells as well as compatibility with various clinically applicable delivery routes of in vivo gene therapy. Therapeutic efficacy was demonstrated in two animal models. To exemplify disease treatments that require on-demand drug secretion, we show that a custom-designed gene switch triggered by the FDA-approved drug grazoprevir can effectively control insulin expression and restore glucose homeostasis in diabetic mice. For diseases that require instantaneous sense-and-response treatment programs, we create highly specific sensors for various subcellularly (mis)localized protein markers (such as cancer-related fusion proteins) and show that translation-based protein sensors can be used either alone or in combination with other cell-state classification strategies to create therapeutic biocomputers driving self-sufficient elimination of tumor cells in mice. This design strategy demonstrates unprecedented flexibility for translational regulation and could form the basis for a novel class of programmable gene therapies in vivo. 

文獻(xiàn)鏈接：https://www.nature.com/articles/s41422-023-00896-y

 

2、ADVANCED MATERIALS（IF=29.4)

 

文獻(xiàn)引用產(chǎn)品：

 

 

 

 

 

 

 

 

 

 

貨號	名稱	CAS	規(guī)格
Y35467	透明質(zhì)酸酶	37326-33-3	≥ 300 IU/mg, from bovine testes
S22118	透明質(zhì)酸酶	37326-33-3	BR, 3000u/mg
S25991	二硬脂?；字Ｒ掖及?聚乙二醇2000	147867-65-0	≥95%
B28313	大豆卵磷脂	8002-43-5	分析標(biāo)準(zhǔn)品,98%
B20272	膽固醇	57-88-5	分析標(biāo)準(zhǔn)品, HPLC≥98%
R31047	伊文思藍(lán)染色液	/	2%

 

 

 

 

 

 

 

 

 

 

 

摘要：The therapy of solid tumors is often hindered by the compact and rigid tumoral extracellular matrix (TECM). Precise reduction of TECM by hyaluronidase (HAase) in combination with nanotechnology is promising for solid tumor therapeutics, yet remains an enormous challenge. Inspired by the treatment of iron poisoning, here a remotely unwrapping strategy is proposed of metal-polyphenol-packaged HAase (named PPFH) by sequentially injecting PPFH and a clinically used iron-chelator deferoxamine (DFO). The in situ dynamic disassembly of PPFH can be triggered by the intravenously injected DFO, resulting in the release, reactivation, and deep penetration of encapsulated HAase inside tumors. Such a cost-effective HAase delivery strategy memorably improves the subsequent photothermal and photodynamic therapy (PTT/PDT)-induced intratumoral infiltration of cytotoxic T lymphocyte cells and the cross-talk between tumor and tumor-draining lymph nodes (TDLN), thereby decreasing the immunosuppression and optimizing tumoricidal immune response that can efficiently protect mice from tumor growth, metastasis, and recurrence in multiple mouse cancer models. Overall, this work presents a proof-of-concept of the dynamic disassembly of metal-polyphenol nanoparticles for extracellular drug delivery as well as the modulation of TECM and immunosuppressive tumor microenvironment.

文獻(xiàn)鏈接：https://onlinelibrary.wiley.com/doi/abs/10.1002/adma.202310673

 

 

 

 

  3、Cell Metabolism（IF=29)

 文獻(xiàn)引用產(chǎn)品:

 

 

 

 

貨號	產(chǎn)品名稱	CAS	規(guī)格
S51482	3-吲哚乙酰胺	879-37-8	98%

 摘要：The brain and gut are intricately connected and respond to various stimuli. Stress-induced brain-gut communication is implicated in the pathogenesis and relapse of gut disorders. The mechanism that relays psychological stress to the intestinal epithelium, resulting in maladaptation, remains poorly understood. Here, we describe a stress-responsive brain-to-gut metabolic axis that impairs intestinal stem cell (ISC) lineage commitment. Psychological stress-triggered sympathetic output enriches gut commensal Lactobacillus murinus, increasing the production of indole-3-acetate (IAA), which contributes to a transferrable loss of intestinal secretory cells. Bacterial IAA disrupts ISC mitochondrial bioenergetics and thereby prevents secretory lineage commitment in a cell-intrinsic manner. Oral α-ketoglutarate supplementation bolsters ISC differentiation and confers resilience to stress-triggered intestinal epithelial injury. We confirm that fecal IAA is higher in patients with mental distress and is correlated with gut dysfunction. These findings uncover a microbe-mediated brain-gut pathway that could be therapeutically targeted for stress-driven gut-brain comorbidities.

 

 

 

 

 

  

 

 

 

 

文獻(xiàn)鏈接：https://www.cell.com/cell-metabolism/pdf/S1550-4131(23)00477-1.pdf