美国Seracare血清线性盘（Linearity Panels）

广州健仑生物科技有限公司

SeraCare Life Sciences公司主要在美国、欧洲和亚洲提供促进人类和动物诊断和治疗学的探索、开发和生产的产品和服务。其业务分为两个部分：诊断和生物制药产品和生物服务。诊断和生物制药产品部门生产和销售诊断和控制面板产品，用于测试传染性疾病的临床实验室及员工培训和能力测试。生物服务部门提供生物银行、来样加工和测试服务。

美国SeraCare收购BBI公司，即原BBI血清盘已经改名为SeraCare血清盘。

其产品包括有：传染病阳性质控品、疾病标准品、细菌阳性质控品、人血清白蛋白、人伽马球蛋白、牛血清白蛋白、血清盘、人血浆、人血清。

SeraCare的血清盘包括：HIV-1转化盘、HIV性能盘、HBV转化盘、HBV性能盘、HCV转化盘、HCV性能盘、弓形虫性能盘、线性盘和质控盘等等。

我司还提供其它进口或国产试剂盒：登革热、疟疾、流感、A链球菌、合胞病毒、腮病毒、乙脑、寨卡、黄热病、基孔肯雅热、克锥虫病、违禁品滥用、肺炎球菌、军团菌、化妆品检测、食品安全检测等试剂盒以及日本生研细菌分型诊断血清、德国SiFin诊断血清、丹麦SSI诊断血清等产品。

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美国Seracare血清线性盘（Linearity Panels）

美国

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【公司名称】 广州健仑生物科技有限公司

【市 场 部】    杨永汉

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【腾讯Q Q】 2042552662

【公司地址】 广州清华科技园创新基地番禺石楼镇创启路63号二期2幢101-103室

研究人员发现用来源于细菌细胞壁的脂多糖(LPS)刺激小鼠巨噬细胞能够上调表达tRNA的相关基因的转录。nf-kb是介导炎症信号的一个关键转录因子,LPS处理能够会增强NF-kB的p65亚基与tRNA基因的作用。除此之外，研究人员还发现p65能够直接与RNA聚合酶III复合物中的转录因子TFIIIB相互作用，并且p65过表达会诱导pol III依赖性的转录过程。抑制巨噬细胞内的pol III活性能够阻止巨噬细胞分泌细胞因子并抑制其吞噬作用，这也是巨噬细胞的两个关键功能特征。
这项研究揭示了RNA聚合酶III对巨噬细胞功能的重要调控作用，证明RNA聚合酶III可能对于恶性肿瘤细胞相关的免疫反应具有重要影响。
效应T细胞迁移进入炎症组织会加重组织损伤并会导致炎症性疾病恶化。来自宾夕法尼亚大学的科研人员发现缺少接头蛋白CRK和CRK-like的T细胞会出现黏附性，趋化性下降等特征，并通过实验证明CRK蛋白家族能够选择性调控t细胞黏附性及向效应位点迁移的能力，并提出针对CRK蛋白家族或可开发针对移植物抗宿主病(GVHD)的治疗方法。zui近，这一研究成果在著名临床杂志JCI在线发表。
研究人员利用条件敲除小鼠发现，在缺少CRK和CRK-like蛋白后，T细胞的黏附性，趋化性均出现下降，并且发现CRK和CRK-like这两种蛋白存在大量功能冗余，过表达两者中任一个都能导致两者缺失导致的T细胞功能缺陷得到恢复。研究人员通过对机制研究发现，CRK能够与RAP鸟嘌呤核苷酸交换因子C3G和黏附驻留分子CASL协同作用激活整合素调节性GTPase RAP1。CRK蛋白对效应T细胞向炎症部位迁移至关重要，但不影响效应T细胞向淋巴器官迁移。

The researchers found that stimulation of mouse macrophages with lipopolysaccharide (LPS) derived from the bacterial cell wall upregulates the transcription of related genes that express tRNA. Nf-kb is a key transcription factor that mediates inflammation. LPS treatment can enhance the role of NF-kB p65 subunit and tRNA gene. In addition, the researchers also found that p65 interacts directly with the transcription factor TFIIIB in the RNA polymerase III complex, and that overexpression of p65 induces pol III-dependent transcription. Inhibition of pol III activity in macrophages can prevent macrophages from secreting cytokines and inhibit their phagocytosis, which is also a key feature of macrophages.
This study revealed an important regulatory role of RNA polymerase III in macrophage function, demonstrating that RNA polymerase III may have an important influence on the immune response associated with malignant cells.
The migration of effector T cells into inflammatory tissue can exacerbate tissue damage and lead to the deterioration of inflammatory diseases. Researchers from the University of Pennsylvania found that the lack of the adaptor proteins CRK and CRK-like T cells exhibited features such as adhesion, decreased chemotaxis, and experiments demonstrated that the CRK protein family can selectively regulate t cell adhesion and effector sites. The ability to migrate and propose treatments for the CRK protein family or can be developed for graft-versus-host disease (GVHD). Recently, this research result was published on the well-known clinical journal JCI Online.
Using conditional knockout mice, the researchers found that in the absence of CRK and CRK-like proteins, T cell adhesion and chemotaxis both decreased, and CRK and CRK-like proteins were found to have a lot of functional redundancy. Overexpression of either of them can lead to the restoration of T cell function defects resulting from the loss of both. Through the study of mechanism, the researchers found that CRK can cooperate with RAP guanine nucleotide exchange factor C3G and adhesion resident molecule CASL to activate integrin-regulated GTPase RAP1. The CRK protein is essential for the migration of effector T cells to the site of inflammation but does not affect the migration of effector T cells to the lymphoid organs.