截止目前,引用Bioss产品发表的文献共29281篇,总影响因子141751.15分,发表在Nature, Science, Cell以及Immunity等顶级期刊的文献共68篇,合作单位覆盖了清华、北大、复旦、华盛顿大学、麻省理工学院、东京大学以及纽约大学等国际研究机构上百所。
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近期收录2024年2月引用Bioss产品发表的文献共363篇(图一,绿色柱),文章影响因子(IF) 总和高达2298.3,其中,10分以上文献45篇(图二)。
图一
图二
本文主要分享引用Bioss产品发表文章至Nature, Immunity, Cancer Cell等期刊的5篇 IF>15 的文献摘要,让我们一起欣赏吧。
Molecular Cancer [IF=37.3]
文献引用产品:bsm-33070M
Ki-67 Mouse mA | IHC
作者单位:重庆医科大学
摘要:CircPDHK1 was upregulated in ccRCC tissues and closely related to WHO/ISUP stage, T stage, distant metastasis, VHL mutation and Ki-67 levels. CircPDHK1 had a functional internal ribosome entry site (IRES) and encoded a novel peptide PDHK1-241aa. Functionally, we confirmed that PDHK1-241aa and not the circPDHK1 promoted the proliferation, migration and invasion of ccRCC. Mechanistically, circPDHK1 was activated by HIF-2A at the transcriptional level. PDHK1-241aa was upregulated and interacted with PPP1CA, causing the relocation of PPP1CA to the nucleus. This thereby inhibited AKT dephosphorylation and activated the AKT-mTOR signaling pathway.
Cellular & Molecular Immunology [IF=24.1]
文献引用抗体:
bs-2789R; Tap1 Rabbit pAb | FC
bs-2374R; TAP2 Rabbit pAb | FC
作者单位:北京大学
摘要:CD4+ T cells can "help" or "license" conventional type 1 dendritic cells (cDC1s) to induce CD8+ cytotoxic T lymphocyte (CTL) anticancer responses, as proven in mouse models. We recently identified cDC1s with a transcriptomic imprint of CD4+ T-cell help, specifically in T-cell-infiltrated human cancers, and these cells were associated with a good prognosis and response to PD-1-targeting immunotherapy. Here, we delineate the mechanism of cDC1 licensing by CD4+ T cells in humans. Activated CD4+ T cells produce IFNβ via the STING pathway, which promotes MHC-I antigen (cross-)presentation by cDC1s and thereby improves their ability to induce CTL anticancer responses. In cooperation with CD40 ligand (L), IFNβ also optimizes the costimulatory and other functions of cDC1s required for CTL response induction. IFN-I-producing CD4+ T cells are present in diverse T-cell-infiltrated cancers and likely deliver “help" signals to CTLs locally, according to their transcriptomic profile and colocalization with “helped/licensed" cDCs and tumor-reactive CD8+ T cells. In agreement with this scenario, the presence of IFN-I-producing CD4+ T cells in the TME is associated with overall survival and the response to PD-1 checkpoint blockade in cancer patients.
ADVANCED FUNCTIONAL MATERIALS [IF=19.0]
文献引用产品:bs-4917R
Osteocalcin Rabbit pAb | IF
作者单位:北京大学口腔医院
ACS Nano [IF=17.1]
文献引用抗体:
bs-0292P; BSA-V
D-9106; DAPI
bsm-33070M; Ki-67 Mouse mAb | IF
作者单位:北京大学
Advanced Science [IF=15.1]
文献引用抗体:
bs-0292P-FITC; BSA / FITC | IF
bsm-60235R; Keratin 6 Recombinant Rabbit mAb | IF
作者单位:南方医科大学
摘要:To address current challenges in effectively treating large skin defects caused by trauma in clinical medicine, the fabrication, and evaluation of a novel radially aligned nanofiber scaffold (RAS) with dual growth factor gradients is presented. These aligned nanofibers and the scaffold's spatial design provide many all-around “highways" for cell migration from the edge of the wound to the center area. Besides, the chemotaxis induced by two growth factor gradients further promotes cell migration. Incorporating epidermal growth factor (EGF) aids in the proliferation and differentiation of basal layer cells in the epidermis, augmenting the scaffold's ability to promote epidermal regeneration. Concurrently, the scaffold-bound vascular endothelial growth factor (VEGF) recruits vascular endothelial cells at the wound's center, resulting in angiogenesis and improving blood supply and nutrient delivery, which is critical for granulation tissue regeneration. The RAS+EGF+VEGF group demonstrates superior performance in wound immune regulation, wound closure, hair follicle regeneration, and ECM deposition and remodeling compared to other groups. This study highlights the promising potential of hierarchically assembled nanofiber scaffolds with dual growth factor gradients for wound repair and tissue regeneration applications.