With a SuperBoost tyramide kit, I got excessive and non-specific labeling. What can I do to limit background and acquire a more localized labeling?
To limit background, we recommend performing a pre-blocking step with 3% H2O2 for 60 mins to inactivate endogenous peroxidases. To limit the localization of labeling, we recommend optimizing the final concentration of the primary and secondary antibodies and the dye-tyramide. You may also limit the incubation time of the dye-tyramide on the sample.
How are SuperBoost tyramide kits different from the original TSA labeling kits?
The SuperBoost tyramide kits utilize poly-HRP labeled antibodies. This provides a greater number of horseradish peroxidase (HRP) molecules per antibody. The original kits used antibodies and streptavidin that were directly conjugated with HRP and thus, limited the number per antibody or streptavidin.
REST regulates the cell cycle for cardiac development and regeneration.
Authors:Zhang D, Wang Y, Lu P, Wang P, Yuan X, Yan J, Cai C, Chang CP, Zheng D, Wu B, Zhou B,
Journal:Nat Commun
PubMed ID:29215012
'Despite the importance of cardiomyocyte proliferation in cardiac development and regeneration, the mechanisms that promote cardiomyocyte cell cycle remain incompletely understood. RE1 silencing transcription factor (REST) is a transcriptional repressor of neuronal genes. Here we show that REST also regulates the cardiomyocyte cell cycle. REST binds and represses the cell ... More
Attenuation of Follicular Helper T Cell-Dependent B Cell Hyperactivity by Abatacept Treatment in Primary Sjögren's Syndrome.
Authors:Verstappen GM, Meiners PM, Corneth OBJ, Visser A, Arends S, Abdulahad WH, Hendriks RW, Vissink A, Kroese FGM, Bootsma H,
Journal:Arthritis Rheumatol
PubMed ID:28564491
'To assess the effect of abatacept (CTLA-4Ig), which limits T cell activation, on homeostasis of CD4+ T cell subsets and T cell-dependent B cell hyperactivity in patients with primary Sjögren''s syndrome (SS). Fifteen patients with primary SS treated with abatacept were included. Circulating CD4+ T cell and B cell subsets ... More
Authors:Yao L, Wright MF, Farmer BC, Peterson LS, Khan AM, Zhong J, Gewin L, Hao CM, Yang HC, Fogo AB
Journal:Nephrol Dial Transplant
PubMed ID:31071225
Plasminogen activator inhibitor-1 (PAI-1) expression increases extracellular matrix deposition and contributes to interstitial fibrosis in the kidney after injury. While PAI-1 is ubiquitously expressed in the kidney, we hypothesized that interstitial fibrosis is strongly dependent on fibroblast-specific PAI-1 (fbPAI-1). ... More
Inhibition of retinoic acid signaling induces aberrant pericyte coverage and differentiation resulting in vascular defects in congenital diaphragmatic hernia.
Authors:Kool HM, Bürgisser PE, Edel GG, de Kleer I, Boerema-de Munck A, de Laat I, Chrifi I, Cheng C, van Cappellen WA, Kremers GJ, Tibboel D, Rottier RJ
Journal:Am J Physiol Lung Cell Mol Physiol
PubMed ID:31268349
The mortality and morbidity of patients with congenital diaphragmatic hernia (CDH) is primarily caused by treatment-resistant, persistent pulmonary hypertension. Structural vascular changes, exemplified by extensive muscularization, are already present early in gestation, but the origin of these abnormalities is unknown. Understanding the origin of the vascular defects is important to ... More
Proteolytic Processing of Neuregulin 2.
Authors:Czarnek M, Bereta J
Journal:Mol Neurobiol
PubMed ID:31838721
Neuregulin 2 (NRG2) belongs to the EGF family of growth factors. Most of this family members require proteolytic cleavage to liberate their ectodomains capable of binding and activating their cognate ErbB receptors. To date, most of the studies investigating proteolytic processing of neuregulins focused on NRG1, which was shown to ... More