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      當前位置:首頁  >  新聞資訊  >  【5月文獻戰報】Bioss抗體新增高分文獻精彩呈現

      【5月文獻戰報】Bioss抗體新增高分文獻精彩呈現

      發表時間:2022-06-24  |  點擊率:1998

       

       


      截至目前,引用Bioss產品發表的文獻共18564篇,總影響因子80606.851分,發表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共53篇,合作單位覆蓋了清華、北大、復旦、華盛頓大學、麻省理工學院、東京大學以及紐約大學等國際研究機構上百所。

      我們每月收集引用Bioss產品發表的文獻。若您在當月已發表SCI文章,但未被我公司收集,請致電Bioss,我們將贈予現金鼓勵,金額標準請參考“發文章 領獎金”活動頁面。

      近期收錄2022年5月引用Bioss產品發表的文獻共223篇(圖一,綠色柱),文章影響因子(IF) 總和高達1283.088,其中,20分以上文章2篇,10分以上文獻26篇(圖二)。

      圖一

       

      圖二



      本文主要分享引用Bioss產品發表文章至Nature NanotechnologyImmunityCancer Cell等期刊的8IF>10的文獻摘要,讓我們一起欣賞吧。

       

      Cell [IF=41.584]



       

      文獻引用抗體:bs-6285R

      Anti-PRSS10 pAb

      作者單位:日本東京大學醫學科學研究所微生物學和免疫學系

      摘要Soon after the emergence and global spread of the SARS-CoV-2 Omicron lineage BA.1, another Omicron lineage, BA.2, began outcompeting BA.1. The results of statistical analysis showed that the effective reproduction number of BA.2 is 1.4-fold higher than that of BA.1. Neutralization experiments revealed that immunity induced by COVID vaccines widely administered to human populations is not effective against BA.2, similar to BA.1, and that the antigenicity of BA.2 is notably different from that of BA.1. Cell culture experiments showed that the BA.2 spike confers higher replication efficacy in human nasal epithelial cells and is more efficient in mediating syncytia formation than the BA.1 spike. Furthermore, infection experiments using hamsters indicated that the BA.2 spike-bearing virus is more pathogenic than the BA.1 spike-bearing virus. Altogether, the results of our multiscale investigations suggest that the risk of BA.2 to global health is potentially higher than that of BA.1.

       

       

       


      Cell Stem Cell [IF=24.633]


      文獻引用抗體:bs-2433R-AF555 

      Anti-ATP4B/AF555 pAb; FCM

      作者單位:奧地利科學院分子生物技術研究所

      摘要Adult stem cells constantly react to local changes to ensure tissue homeostasis. In the main body of the stomach, chief cells produce digestive enzymes; however, upon injury, they undergo rapid proliferation for prompt tissue regeneration. Here, we identified p57Kip2 (p57) as a molecular switch for the reserve stem cell state of chief cells in mice. During homeostasis, p57 is constantly expressed in chief cells but rapidly diminishes after injury, followed by robust proliferation. Both single-cell RNA sequencing and dox-induced lineage tracing confirmed the sequential loss of p57 and activation of proliferation within the chief cell lineage. In corpus organoids, p57 overexpression induced a long-term reserve stem cell state, accompanied by altered niche requirements and a mature chief cell/secretory phenotype. Following the constitutive expression of p57 in vivo, chief cells showed an impaired injury response. Thus, p57 is a gatekeeper that imposes the reserve stem cell state of chief cells in homeostasis.

       

       

       


      human reproduction update 

      [IF=15.61]


      文獻引用抗體:bs-2734R 
      Anti-Bcl-6 pAb; IHC
      作者單位:法蘭克福大學醫院婦產科產前和產科醫學部

      摘要
      BACKGROUND
      The key oncogene B-cell lymphoma 6 (BCL6) drives malignant progression by promoting proliferation, overriding DNA damage checkpoints and blocking cell terminal differentiation. However, its functions in the placenta and the endometrium remain to be defined.
      OBJECTIVE AND RATIONALE
      Recent studies provide evidence that BCL6 may play various roles in the human placenta and the endometrium. Deregulated BCL6 might be related to the pathogenesis of pre-eclampsia (PE) as well as endometriosis. In this narrative review, we aimed to summarize the current knowledge regarding the pathophysiological role of BCL6 in these two reproductive organs, discuss related molecular mechanisms, and underline associated research perspectives .....

       

      Small [IF=13.281]


      文獻引用抗體:

      bs-4842R 

      Anti-Phospho-EIF2S1(Ser51) pAb

      bs-1136R 
      Anti-Synaptotagmin-2 pAb
      作者單位:天津大學藥學科技學院天津重點實驗室

      摘要To overcome the autophagy compromised mechanism of protective cellular processes by “eating”/“digesting” damaged organelles or potentially toxic materials with autolysosomes in tumor cells, lysosomal impairment can be utilized as a traditional autophagy dysfunction route for tumor therapy; however, this conventional one-way autophagy dysfunction approach is always limited by the therapeutic efficacy. Herein, an innovative pharmacological strategy that can excessively provoke autophagy via endoplasmic reticulum (ER) stress is implemented along with lysosomal impairment to enhance autophagy dysfunction. In this work, the prepared tellurium double-headed nanobullets (TeDNBs) with controllable morphology are modified with human serum albumin (HSA) which facilitates internalization by tumor cells. On the one hand, ER stress can be stimulated by upregulating the phosphorylation eukaryotic translation initiation factor 2 (P-eIF2α) owing to the production of tellurite(TeO32-) in the specifical hydrogen peroxide-rich tumor environment; thus, autophagy overstimulation occurs. On the other hand, OME can deacidify and impair lysosomes by downregulating lysosomal-associated membrane protein 1 (LAMP1), therefore blocking autolysosome formation. Both in vitro and in vivo results demonstrate that the synthesized TeDNBs-HSA/OME (TeDNBs-HO) exhibit excellent therapeutic efficacy by autophagy dysfunction through ER stress induction and lysosomal damnification. Thus, TeDNBs-HO is verified to be a promising theranostic nanoagent for effective tumor therapy.

       

      Biomaterials [IF=12.479]


      文獻引用抗體:bs-2593R

      Anti-Caspase 3 precursor pAb; IF

      作者單位:蘇州大學蘇州醫學院,江蘇省高等學校放射醫學與防護國家重點實驗室(RAD-X) 輻射醫學合作創新中心

      摘要Apoptosis dysregulation is an important mechanism responsible for the intrinsic and acquired resistance of melanoma, which necessitates the exploration of oncological treatments to activate nonapoptotic cell death. Herein, we developed nano-enabled photosynthesis in tumours to activate lipid peroxidation and ferroptosis to overcome melanoma resistance. Controlled photosynthesis was conducted in tumours to construct a hyperoxic microenvironment with photosynthetic microcapsules (PMCs), which were prepared by encapsulating cyanobacteria and upconversion nanoparticles in alginate microcapsules and driven by external near infrared photons. The combination of PMCs and X-rays evoked lipid peroxidation, Fe2+ release, glutathione peroxidase 4 suppression, glutathione reduction and ferroptosis in melanoma cells and xenografts. Consequently, the intrinsic and acquired resistance in melanoma could be overcome by the combined treatment, which further inhibited tumour metastases and improved the survival rate of melanoma-bearing mice. Overall, the development of nano-enabled photosynthesis in tumours will inspire the exploration of oncological treatments.

       

      progress in neurobiology

      [IF=11.685]


      文獻引用抗體:
      bs-3504R
      Anti-MST1 pAb; IB

      bs-4635R

      Anti-Phospho-MST1 (Thr183) pAb; IB, IF

      作者單位:南開大學生命科學學院

      摘要Alzheimer’s disease (AD) is the most prevalent form of dementia in the old adult and characterized by progressive cognitive decline and neuronal damage. The mammalian Ste20-like kinase1/2 (MST1/2) is a core component in Hippo signaling, which regulates neural stem cell proliferation, neuronal death and neuroinflammation. However, whether MST1/2 is involved in the occurrence and development of AD remains unknown. In this study we reported that the activity of MST1 was increased with Aβ accumulation in the hippocampus of 5xFAD mice. Overexpression of MST1 induced AD-like phenotype in normal mice and accelerated cognitive decline, synaptic plasticity damage and neuronal apoptosis in 2-month-old 5xFAD mice, but did not significantly affect Aβ levels. Mechanistically, MST1 associated with p53 and promoted neuronal apoptosis by phosphorylation and activation of p53, while p53 knockout largely reversed MST1-induced AD-like cognitive deficits. Importantly, either genetic knockdown or chemical inactivation of MST1 could significantly improve cognitive deficits and neuronal apoptosis in 7-month-old 5xFAD mice. Our results support the idea that MST1-mediated neuronal apoptosis is an essential mechanism of cognitive deficits and neuronal loss for AD, and manipulating the MST1 activity as a potential strategy will shed light on clinical treatment for AD or other diseases caused by neuronal injury.


       

      BIOENGINEERING &

      TRANSLATIONAL MEDICINE

      [IF=10.711]


      文獻引用抗體:bs-0195R 

      Anti-CD31 pAb; WB
      作者單位:廣州中醫藥大學

      摘要Abnormal endometrial receptivity is a major cause of the failure of embryo transplantation, which may lead to infertility, adverse pregnancy, and neonatal outcomes. While hormonal treatment has dramatically improved the fertility outcomes in women with endometriosis, a substantial unmet need persists in the treatment. In this study, methacrylate gelatin (GelMA) and methacrylate sericin (SerMA) hydrogel with human umbilical cord mesenchymal stem cells (HUMSC) encapsulation was designed for facilitating endometrial regeneration and fertility restoration through in situ injection. The presented GelMA/10%SerMA hydrogel showed appropriate swelling ratio, good mechanical properties, and degradation stability. In vitro cell experiments showed that the prepared hydrogels had excellent biocompatibility and cell encapsulation ability of HUMSC. Further in vivo experiments demonstrated that GelMA/SerMA@HUMSC hydrogel could increase the thickness of endometrium and improve the endometrial interstitial fibrosis. Moreover, regenerated endometrial tissue was more receptive to transfer embryos. Summary, we believed that GelMA/SerMA@HUMSC hydrogel will hold tremendous promise to repair or regenerate damaged endometrium.


       

      kidney INTERNATIONAL

      [IF=10.612]


      文獻引用抗體:bs-0666R

      Anti-Fibronectin/FN1 pAb

      作者單位:日本東京日慶大學醫學院內科糖尿病、代謝和內分泌科

      摘要Dysregulation of fatty acid utilization is increasingly recognized as a significant component of diabetic kidney disease. Rho-associated, coiled-coil–containing protein kinase (ROCK) is activated in the diabetic kidney, and studies over the past decade have illuminated ROCK signaling as an essential pathway in diabetic kidney disease. Here, we confirmed the distinct role of ROCK1, an isoform of ROCK, in fatty acid metabolism using glomerular mesangial cells and ROCK1 knockout mice. Mesangial cells with ROCK1 deletion were protected from mitochondrial dysfunction and redox imbalance driven by transforming growth factor β, a cytokine upregulated in diabetic glomeruli. We found that high-fat diet-induced obese ROCK1 knockout mice exhibited reduced albuminuria and histological abnormalities along with the recovery of impaired fatty acid utilization and mitochondrial fragmentation. Mechanistically, we found that ROCK1 regulates the induction of critical mediators in fatty acid metabolism, including peroxisome proliferator-activated receptor gamma coactivator 1α, carnitine palmitoyltransferase 1, and widespread program-associated cellular metabolism. Thus, our findings highlight ROCK1 as an important regulator of energy homeostasis in mesangial cells in the overall pathogenesis of diabetic kidney disease.

       

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