By in News ,Press release

Hard work, Do not forget your initiative mind- Abbkine Added 210 Citations in April

In April 2020, Abbkine collected 210 English articles published using Abbkine products, and some of them sent us good news on their own initiative. The joy was beyond words. In this collection of articles, the highest impact factor (IF) is 13.05, with articles with IF>7 accounting for 10.4% and articles with IF>4 accounting for 43%.

In the current evaluation of scientific research, scientific research papers, as the systematic summary and theoretical crystallization of scientific research carried out by scientific researchers, are still the main objects for measuring innovative activities, especially basic research activities. Science, Nature and Cell are internationally recognized journals with the highest academic reputation. According to the statistical results of Chinese scientific papers in 2018, the number of Chinese papers published in the above three journals in 2017 was 309, an increase of 11 articles over the previous year, ranking fourth in the world. China's scientific research strength should not be underestimated!

Let's take a look at some of the research workers in China who are studying some topics.

Title: MST4 kinase suppresses gastric tumorigenesis by limiting YAP activation via a non-canonical pathway

Magazine: Journal of Experimental Medicine

Impact factor: 9.83

University: Tongji University

Abstract: Hyperactivation of YAP has been commonly associated with tumorigenesis, and emerging evidence hints at multilayered Hippo-independent regulations of YAP. In this study, we identified a new MST4–YAP axis, which acts as a noncanonical Hippo signaling pathway that limits stress-induced YAP activation. MST4 kinase directly phosphorylated YAP at Thr83 to block its binding with importin α, therefore leading to YAP cytoplasmic retention and inactivation. Due to a consequential interplay between MST4-mediated YAP phospho-Thr83 signaling and the classical YAP phospho-Ser127 signaling, the phosphorylation level of YAP at Thr83 was correlated to that at Ser127. Mutation of T83E mimicking MST4-mediated alternative signaling restrained the activity of both wild-type YAP and its S127A mutant mimicking loss of classical Hippo signal. Depletion of MST4 in mice promoted gastric tumorigenesis with diminished Thr83 phosphorylation and hyperactivation of YAP. Moreover, loss of MST4–YAP signaling was associated with poor prognosis of human gastric cancer. Collectively, our study uncovered a noncanonical MST4–YAP signaling axis essential for suppressing gastric tumorigenesis.

Article link: https://rupress.org/jem/article/217/6/e20191817/151647

Products using from Abbkine:

 IPKine™ HRP, Goat Anti-Mouse IgG LCS (CAT#A25012)

IPKine™ HRP, Mouse Anti-Rabbit IgG LCS (CAT#A25022)

Title: TRIM32/USP11 Balances ARID1A Stability and the Oncogenic/Tumor-Suppressive Status of Squamous Cell Carcinoma

Magazine: Cell Reports

Impact factor: 8.04

University: Chinese Academy of Medical Sciences and Peking Union Medical College

Abstract: Squamous cell carcinoma (SCC) is an aggressive epithelial malignancy, yet the molecular mechanisms underlying SCC development are elusive. ARID1A is frequently mutated in various cancer types, but both mutation rates and expression levels of ARID1A are ubiquitously low in SCCs. Here, we reveal that excessive protein degradation mediated by the ubiquitin-proteasome system (UPS) contributes to the loss of ARID1A expression in SCC. We identify that the E3 ligase TRIM32 and the deubiquitinase USP11 play key roles in controlling ARID1A stability. TRIM32 depletion inhibits SCC cell proliferation, metastasis, and chemoresistance by stabilizing ARID1A, while USP11 depletion promotes SCC development by promoting ARID1A degradation. We show that syndecan-2 (SDC2) is the downstream target of both ARID1A and USP11 and that SDC2 depletion abolishes the oncogenic function of ARID1A loss. In summary, our data reveal UPS-mediated protein degradation as a mechanism underlying ARID1A loss and propose an important role for the TRIM32/USP11-ARID1A-SDC2 axis in SCC.

Article link: https://www.sciencedirect.com/science/article/pii/S2211124719316675

Products using from Abbkine:

ExKineTM Nuclear and Cytoplasmic Protein Extraction Kit (CAT#KTP3001)

Title: Microneedle drug eluting balloon for enhanced drug delivery to vascular tissue

Magazine: Journal of Controlled Release

Impact factor: 7.82

University: Yonsei University, Seoul

Abstract: High rates of restenosis and neointimal formation have driven increasing interest in the application of drug eluting balloons (DEB) as counteractive measures for intraluminal drug delivery. The use of DEBs eliminates the need for stents so that serious side effects including in-stent restenosis and stent thrombosis can be avoided and long-term medication of antiplatelet agent is not needed. Despite their benefits, DEBs have poor drug delivery efficiency due to short balloon inflation times (30~60 seconds) that limit the passive drug diffusion from the balloon surface to the luminal lesion. To increase drug delivery efficiency, a microneedle DEB (MNDEB) was developed by a conformal transfer molding process using a thin polydimethylsiloxane mold bearing a negative array of MNs of 200 μm in height. A MN array composed of UV curable resin was formed onto the surface of DEB, and drugs were coated onto the structure. The mechanical properties of the MN array were investigated and MN

penetration into luminal vasculature was confirmed in vivo. An increase in drug delivery efficiency compared to a standard DEB was demonstrated in an in vivo test in a rabbit aorta. Finally, the superior therapeutic efficacy of MNDEBs was evaluated using an atherosclerosis rabbit model.

Article link: https://www.sciencedirect.com/science/article/abs/pii/S0168365920300894

Products using from Abbkine:

EliKine™ Mouse IL-1β ELISA Kit (CAT#KET7005)

EliKine™ Mouse TNF-α ELISA Kit (CAT#KET7015)

Title: Polyphyllin VI Induces Caspase-1-Mediated Pyroptosis via the Induction of ROS/NF-κB/NLRP3/GSDMD Signal Axis in Non-Small Cell Lung Cancer

Magazine: Cancers

Impact factor: 5.87

University: Southwest Medical University

Abstract: Trillium tschonoskii Maxim (TTM), a traditional Chinese medicine, has been demonstrated to have a potent anti-tumor effect. Recently, polyphyllin VI (PPVI), a main saponin isolated from TTM, was reported by us to significantly suppress the proliferation of non-small cell lung cancer (NSCLC) via the induction of apoptosis and autophagy in vitro and in vivo. In this study, we further found that the NLRP3 inflammasome was activated in PPVI administrated A549-bearing athymic nude mice. As is known to us, pyroptosis is an inflammatory form of caspase-1-dependent programmed cell death that plays an important role in cancer. By using A549 and H1299 cells, the in vitro effect and action mechanism by which PPVI induces activation of the NLRP3 inflammasome in NSCLC were investigated. The anti-proliferative effect of PPVI in A549 and H1299 cells was firstly measured and validated by MTT assay. The activation of the NLRP3 inflammasome was detected by using Hoechst33324/PI staining, flow cytometry analysis and real-time live cell imaging methods. We found that PPVI significantly increased the percentage of cells with PI signal in A549 and H1299, and the dynamic change in cell morphology and the process of cell death of A549 cells indicated that PPVI induced an apoptosis-to-pyroptosis switch, and, ultimately, lytic cell death. In addition, belnacasan (VX-765), an inhibitor of caspase-1, could remarkably decrease the pyroptotic cell death of PPVI-treated A549 and H1299 cells. Moreover, by detecting the expression of NLRP3, ASC, caspase-1, IL-1β, IL-18 and GSDMD in A549 and h1299 cells using Western blotting, immunofluorescence imaging and flow cytometric analysis, measuring the caspase-1 activity using colorimetric assay, and quantifying the cytokines level of IL-1β and IL-18 using ELISA, the NLRP3 inflammasome was found to be activated in a dose manner, while VX-765 and necrosulfonamide (NSA), an inhibitor of GSDMD, could inhibit PPVI-induced activation of the NLRP3 inflammasome. Furthermore, the mechanism study found that PPVI could activate the NF-κB signaling pathway via increasing reactive oxygen species (ROS) levels in A549 and H1299 cells, and N-acetyl-L-cysteine (NAC), a scavenger of ROS, remarkably inhibited the cell death, and the activation of NF-κB and the NLRP3 inflammasome in PPVI-treated A549 and H1299 cells. Taken together, these data suggested that PPVI-induced, caspase-1-mediated pyroptosis via the induction of the ROS/NF-κB/NLRP3/GSDMD signal axis in NSCLC, which further clarified the mechanism of PPVI in the inhibition of NSCLC, and thereby provided a possibility for PPVI to serve as a novel therapeutic agent for NSCLC in the future

Article link: https://www.mdpi.com/2072-6694/12/1/193

Products using from Abbkine:

Caspase-1 Assay Kit (Colorimetric) (CAT#KTA3020)

Title: Integrin β3 promotes cardiomyocyte proliferation and attenuates hypoxia-induced apoptosis via regulating the PTEN/Akt/mTOR and ERK1/2 pathways

Magazine: International Journal of Biological Sciences

Impact factor: 4.04

University: Shanghai Jiaotong University

Article link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6990915/

Abstract: Integrin β3 is one of the main integrin heterodimer receptors on the surface of cardiac myocytes. Our previous studies showed that hypoxia induces apoptosis and increases integrin β3 expression in cardiomyocytes. However, the exact mechanism by which integrin β3 protects against apoptosis remains unclear. Hence, the present investigation aimed to explore the mechanism of integrin β3 in cardiomyocyte proliferation and hypoxia-induced cardiomyocyte apoptosis.

Products using from Abbkine:

Annexin V-AbFluor™ 555 Apoptosis Detection kit (CAT#KTA0003)