Sentence examples for nsc control from inspiring English sources

We first established two NSC lines from the SVZ of early symptomatic C57BL6 IDS-ko mice and two NSC control lines from wild-type (wt) syngenic littermates.

(F ) ICC for the neuronal marker Tuj1 and the astrocyte marker GFAP of SVZ NSC control and Ezh2 Δ/Δ cultures after 7 days of differentiation.

Chromatin immunoprecipitation (ChIP) analysis indicated that Sox2, HDAC1, dimethylation of histone H3 lysine 9 (Met-K9) and heterochromatin protein-1 (HP1) were associated on the endogenous NeuroD1 promoter, suggesting a repressive chromatin state in NSCs (control, Fig S6F of Supporting information).

To confirm SOX2, TLX, and FGFR-2 expression in melatonin treated NSCs and control NSCs, reverse transcription- (RT-) PCR was performed using SOX2-specific primers and TLX-specific primers.

Exposure to the inhibitor was sufficient to reduce the number of pSTAT3-IR cells and to restore the number of Tuj1-, GFAP- and NG2-IR cells in mutant postnatal NSCs to control levels (Fig. 7A), also in differentiated postnatal NSC-derived cultures (Fig. 7B).

We observed accumulated macrophage/microglia in the infarcted cortex and striatum in both FePro-NSC and control groups, and some of them co-labelled with iron.

Interestingly, mTORC1 inhibition by rapamycin reduced pS6 activation and reverted the premature glial differentiation in mutant postnatal NSCs to control levels (Fig. 6F).

Although we detected a slight increase in apoptosis (7 8%) at 24 h after FE-Pro labeling, the proportion of apoptotic cells in FE-Pro-labeled NSCs decreased to a level comparable to the non-labeled control NSCs (5%) at later stages of NSC culture (up to 9 days).

Neurospheres from Nestin-Cre/N2ICD NSCs were significantly larger than those from control NSCs (73.1±2.4 μm, n=226 neurospheres versus 42.56±1.08 μm, n=224 neurospheres, mean diameter±S.E.M., P<0.0001), indicating that N2ICD expression increases NSC proliferation in neurospheres, similar as in vivo.

Quantitative PCR (SYBR-Green based; LC480 instrument) using four internal NimbleGen control loci NSC-02377, NSC-0247, NSC-0268, NSC-0272) was performed to estimate relative fold-enrichment (data not shown).

Using BrdU incorporation, no differences were observed in the proliferation of either Sox1+/Nestin− early NSCs derived from control and all Rest mutants or in Sox1+/Nestin+ late NSCs derived from the control, REST/KD-50 and REST-null+REST ES cells.