Human ENG ELISA Matched Antibody Pair (ABPR-0294)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Species Reactivity
Intended Use
This antibody pair set comes with matched antibody pair to detect and quantify protein level of human ENG.
General Description
This gene encodes a homodimeric transmembrane protein which is a major glycoprotein of the vascular endothelium. This protein is a component of the transforming growth factor beta receptor complex and it binds to the beta1 and beta3 peptides with high affinity. Mutations in this gene cause hereditary hemorrhagic telangiectasia, also known as Osler-Rendu-Weber syndrome 1, an autosomal dominant multisystemic vascular dysplasia. This gene may also be involved in preeclampsia and several types of cancer. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
Reconstitution And Storage
Store reagents of the antibody pair set at -20°C or lower. Please aliquot to avoid repeated freeze thaw cycle. Reagents should be returned to -20°C storage immediately after use.


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Forced Convection Heat Transfer From a Particle at Small and Large Peclet Numbers


Authors: Dehdashti, Esmaeil; Masoud, Hassan

We theoretically study forced convection heat transfer from a single particle in uniform laminar flows. Asymptotic limits of small and large Peclet numbers Pe are considered. For Pe << 1 (diffusion-dominated regime) and a constant heat flux boundary condition on the surface of the particle, we derive a closed-form expression for the heat transfer coefficient that is valid for arbitrary particle shapes and Reynolds numbers, as long as the flow is incompressible. Remarkably, our formula for the average Nusselt number Nu has an identical form to the one obtained by Brenner for a uniform temperature boundary condition (Chem. Eng. Sci., vol. 18, 1963, pp. 109-122). We also present a framework for calculating the average Nu of axisymmetric and two-dimensional (2D) objects with a constant heat flux surface condition in the limits of Pe >> 1 and small or moderate Reynolds numbers. Specific results are presented for the heat transfer from spheroidal particles in Stokes flow.

Comprehensive identification of signaling pathways for idiopathic pulmonary arterial hypertension


Authors: Liu, Bingxun; Zhu, Liping; Yuan, Ping; Marsboom, Glenn; Hong, Zhigang; Liu, Jinming; Zhang, Peng; Hu, Qinghua

Whole exome sequencing (WES) was used in the research of familial pulmonary arterial hypertension (FPAH). CAV1 and KCNK3 were found as two novel candidate genes of FPAH. However, few pathogenic genes were identified in idiopathic pulmonary arterial hypertension (IPAH). We conducted WES in 20 unrelated IPAH patients who did not carry the known PAH-pathogenic variants among BMPR2, CAV1, KCNK3, SMAD9, ALK1, and ENG. We found a total of 4,950 variants in 3,534 genes, including 4,444 single-nucleotide polymorphisms and 506 insertions/deletions (InDels). Through the comprehensive and multilevel analysis, we disclosed several novel signaling cascades significantly connected to IPAH, including variants related to cadherin signaling pathway, dilated cardiomyopathy, glucose metabolism, immune response, mucin-type O-glycosylation, phospholipase C (PLC)-activating G protein-coupled receptor (GPCR) signaling pathway, vascular contraction and generation, and voltage-dependent Ca2+ channels. We also conducted validation studies in five mutant genes related to PLC-activating GPCR signaling pathway potentially involved in intracellular calcium regulation through Sanger sequencing for mutation accuracy, qRT-PCR for mRNA stability, immunofluorescence for subcellular localization, Western blotting for protein level, Fura-2 imaging for intracellular calcium, and proliferation analysis for cell function. The validation experiments showed that those variants in CCR5 and C3AR1 significantly increased the rise of intracellular calcium and the variant in CCR5 profoundly enhanced proliferative capacity of human pulmonary artery smooth muscle cells. Thus, our study suggests that multiple genetically affected signaling pathways take effect together to cause the formation of IPAH and the development of right heart failure and may further provide new therapy targets or putative clues for the present treatments such as limited therapeutic effectiveness of Ca2+ channel blockers.

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