NeuroTACS In Situ Apoptosis Detection Kit
NeuroTACS In Situ Apoptosis Detection Kit SummaryProvides rapid and convenient identification of apoptosis in brain tissue or neuronal cells using a TUNEL based assay.
• Unique buffer system produces more consistent labeling.
• Performance tested on brain sections.
• Includes exclusive NeuroPore permeabilization reagent.
• Includes TACS-Nuclease solution for preparing sample-dependent positive controls.
• Helps resolve unique problems encountered when detecting apoptotic neuronal cells.
Why Use the NeuroTACS In Situ Apoptosis Detection Kit?
The kit has been developed to overcome the common difficulties unique to neuronal samples including the fragile nature of brain tissue sections, high background problems, poor counterstaining with common dyes, and the need to perform dual labeling experiments to detect cell specific antigens in conjunction with apoptotic cells. A key feature is NeuroPore, a proprietary permeabilization reagent that gently permeabilizes samples while retaining cell morphology. NeuroPore also contains blocking reagents to allow its use as an antibody diluent in immunohistochemistry and to reduce background staining.
• Proteinase K
• DAB Enhancer
• TACS-Nuclease Buffer
• TACS 2 TdT Labeling Buffer
• TACS 2 TdT Stop Buffer
• TACS 2 TdT dNTP
• TdT Enzyme
• 50x Manganese Cation
• Blue Counterstain
For research use only. Not for diagnostic use.
Citations for NeuroTACS In Situ Apoptosis Detection Kit
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.
Citations: Showing 1 - 8
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Zebrafish Blunt-Force TBI Induces Heterogenous Injury Pathologies That Mimic Human TBI and Responds with Sonic Hedgehog-Dependent Cell Proliferation across the Neuroaxis
Authors: J Hentig, K Cloghessy, M Lahne, YJ Jung, RA Petersen, AC Morris, DR Hyde
Biomedicines, 2021;9(8):. 2021
Synaptic synthesis, dephosphorylation, and degradation: a novel paradigm for an activity-dependent neuronal control of CDKL5.
Authors: La Montanara P, Rusconi L, Locarno A, Forti L, Barbiero I, Tramarin M, Chandola C, Kilstrup-Nielsen C, Landsberger N
J Biol Chem, 2015;290(7):4512-27. 2015
Microcirculatory, mitochondrial, and histological changes following cerebral ischemia in swine.
Authors: Suchadolskiene, Olga, Pranskunas, Andrius, Baliutyte, Giedre, Veikutis, Vincenta, Dambrauskas, Zilvinas, Vaitkaitis, Dinas, Borutaite, Vilmante
BMC Neurosci, 2014;15(0):2. 2014
Chronic application of nonylphenol-induced apoptosis via suppression of bcl-2 transcription and up-regulation of active caspase-3 in mouse brain.
Authors: Mao Z, Zheng YL, Zhang YQ, Han BP, Chen LT, Li J, Li F, Shan Q
Neurosci. Lett., 2008;439(2):147-52. 2008
Hypoxia inducible factor-1alpha (HIF-1alpha) is required for neural stem cell maintenance and vascular stability in the adult mouse SVZ.
Authors: Li L, Candelario K, Thomas K, Wang R, Wright K, Messier A, Cunningham L
J Neurosci, 0;34(50):16713-9. 0
Differences in the phagocytic response of microglia and peripheral macrophages after spinal cord injury and its effects on cell death.
Authors: Greenhalgh A, David S
J Neurosci, 0;34(18):6316-22. 0
Impaired autophagy in neurons after disinhibition of mammalian target of rapamycin and its contribution to epileptogenesis.
Authors: McMahon J, Huang X, Yang J, Komatsu M, Yue Z, Qian J, Zhu X, Huang Y
J Neurosci, 0;32(45):15704-14. 0
The splicing regulator Rbfox2 is required for both cerebellar development and mature motor function.
Authors: Gehman L, Meera P, Stoilov P, Shiue L, O'Brien J, Meisler M, Ares M, Otis T, Black D
Genes Dev, 0;26(5):445-60. 0
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