NSC 26646-d6 - CAS 221093-41-0
Main Product
Product Name:
NSC 26646-d6
Catalog Number:
(16β,17β)-Estra-1,3,5(10)-triene-3,16,17-triol-d6; Estra-1,3,5(10)-triene-3,16β,17β-triol-d6; 16-Epiestratriol-d6; 16β,17β-Estriol-d6; 16β-Hydroxyestradiol-d6; Actriol-d6
CAS Number:
Molecular Weight:
Molecular Formula:
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Chemical Structure
CAS 221093-41-0 NSC 26646-d6

Reference Reading

1.Porf-2 Inhibits Neural Stem Cell Proliferation Through Wnt/β-Catenin Pathway by Its GAP Domain.
Huang GH1, Yang XT1, Chen K1, Xing J1, Guo L2, Zhu L1, Li HJ1, Li XC1, Zhang SY1, Feng DF3. Front Cell Neurosci. 2016 Mar 31;10:85. doi: 10.3389/fncel.2016.00085. eCollection 2016.
Neural stem cell (NSC) proliferation and differentiation play a pivotal role in the development of brain, the plasticity of the brain network, and the repair for brain function in CNS diseases. The mechanisms regulating NSC behavior are not well elucidated. Previous studies showed porf-2 functions as a modulator in central nerve system development. We here show that porf-2, a conserved family of RhoGAPs, is highly and specifically expressed in NSCs. We also demonstrate that porf-2 inhibits the proliferation of NSCs in vivo and in vitro, but has no effect on NSC differentiation. We investigated which domain is required for the role of porf-2 on NSC proliferation. By using neurosphere formation and Edu assay we confirmed the GAP domain is necessary for its function. In addition, we surveyed a few classical pathways on NSC proliferation and found that porf-2 inhibits NSC proliferation by suppressing the β-catenin nuclear translocation. Taken together, we show for the first time that porf-2 inhibits NSC proliferation through Wnt/β-catenin pathway by its GAP domain.
2.HIV non-nucleoside reverse transcriptase inhibitor efavirenz reduces neural stem cell proliferation in vitro and in vivo.
Jin J, Grimmig B, Izzo J, Brown LA, Hudson C, Smith AJ, Tan J, Bickford PC, Giunta B. Cell Transplant. 2016 Apr 8. [Epub ahead of print]
The prevalence of HIV associated neurocognitive disorders (HAND) is rising despite combination antiretroviral therapy (cART). There is evidence that neural stem cells (NSCs) can migrate to sites of brain injury such as those caused by inflammation and oxidative stress, which are a pathological features of HAND. Thus, reductions in NSCs may contribute to HAND pathogenesis. Since the HIV non-nucleoside reverse transcriptase inhibitor efavirenz (EFV) has previously been associated with cognitive deficits and promotion of oxidative stress pathways, we examined its effect on NSCs in vitro as well as in C57BL/6 mice. Here we report that EFV induced a decrease in NSC proliferation in vitro as indicated by MTT assay, as well as BrdU and Nestin immunocytochemistry. In addition, EFV decreased intracellular NSC adenosine triphosphate (ATP) stores, and NSC mitochondrial membrane potential (MMP). Further, we found that EFV promoted increased lactate dehydrogenase (LDH) release, activation of p38 MAPK, and increased Bax expression in cultured NSCs.
3.PPARγ Is Activated during Congenital Cytomegalovirus Infection and Inhibits Neuronogenesis from Human Neural Stem Cells.
Rolland M1, Li X2, Sellier Y3,4, Martin H1, Perez-Berezo T1, Rauwel B1, Benchoua A5,6, Bessières B3,4, Aziza J7, Cenac N1, Luo M2, Casper C1,8, Peschanski M5,6, Gonzalez-Dunia D1, Leruez-Ville M3,4, Davrinche C1, Chavanas S1. PLoS Pathog. 2016 Apr 14;12(4):e1005547. doi: 10.1371/journal.ppat.1005547. eCollection 2016.
Congenital infection by human cytomegalovirus (HCMV) is a leading cause of permanent sequelae of the central nervous system, including sensorineural deafness, cerebral palsies or devastating neurodevelopmental abnormalities (0.1% of all births). To gain insight on the impact of HCMV on neuronal development, we used both neural stem cells from human embryonic stem cells (NSC) and brain sections from infected fetuses and investigated the outcomes of infection on Peroxisome Proliferator-Activated Receptor gamma (PPARγ), a transcription factor critical in the developing brain. We observed that HCMV infection dramatically impaired the rate of neuronogenesis and strongly increased PPARγ levels and activity. Consistent with these findings, levels of 9-hydroxyoctadecadienoic acid (9-HODE), a known PPARγ agonist, were significantly increased in infected NSCs. Likewise, exposure of uninfected NSCs to 9-HODE recapitulated the effect of infection on PPARγ activity.