hl

(redirected from HES1)
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References in periodicals archive ?
Effects of Hydrochloric Acid and Deoxycholic Acid on Notch1, Hes1, K13, and MUC2 Expressions.
B, Expression of Notch down-stream gene Hes1 was observed in transfected B16 tumor cells.
Citation: Ines Lahmann et al., Oscillations of MyoD and Hes1 proteins regulate the maintenance of activated muscle stem cells.
Notch and Hes1 were selected based on the previously described function during self-renewal whereby decreased Notch activity leads to differentiation (Duncan et al.
Okada et al., "Transcription factor Hes1 modulates osteoarthritis development in cooperation with calcium/calmodulin-dependent protein kinase 2," Proceedings of the National Academy of Sciences of the United States of America, vol.
Membranes were blocked for 1 h in Tris-buffered saline and Tween 20 (TBST, pH 7.6) containing 5% nonfat dry milk and incubated overnight at 4[degrees]C with antibodies against Notch1 ICD and Hes1 (Abcam, Cambridge, MA), MnSOD (Santa Cruz Biotechnology), JAK2/phospho-JAK2 (Abcam, Cambridge, MA), STAT3/phospho-STAT3, and GAPDH (Cell Signaling Technology, Danvers, MA), followed by washes with TBST.
MicroRNA-199b-5p impairs cancer stem cells through negative regulation of HES1 in medulloblastoma.
Diaz et al., "The glucocorticoid receptor controls hepatic dyslipidemia through Hes1," Cell Metabolism, vol.
PTEN downregulation is modulated by Notch1 through the activation of the transcription factor hair and enhancer of SPLIT (HES1), whereas PTEN upregulation derives from the inhibition of the binding protein suppressor of hairless (RBPJ), also known as CBF-1 [30-32].
Realtime qPCR was performed on a 1-[micro]L sample of cDNA with either TaqMan probes or SybrGreen (both from Life Technologies) using a StepOnePlus Real-Time PCR System (Applied Biosystems, Life Technologies) and the following Taqman Probes: P-Actin, Mm00607939_s1; Tnf, Mm00443260_g1; Notchl, Mm00435249_m 1; Notch2, Mm00803077_m1; Notch3, Mm00435270_ m1; Jag1, Mm00496902_m1; Jag2, Mm01325629_m1; Dll1, Mm01279269_ m1; Hes1, Mm0 1 342805_m1; Cxcl2, Mm00436450_m1.
This effect is mediated by inactivation of the NOTCH1-dependent transcriptional repressor at the HES1 promoter of glucocorticoid receptor genes and subsequent upregulation of the glucocorticoid receptors.
Another study also showed that miR-1 could promote the differentiation of MSCs into cardiac cells by decreasing the expression of Hes1, a Notch pathway target gene [21].
Hes1 is known to be important for maintaining the self-renewal ability of progenitors and repressing the commitment of multipotent progenitor cells to a neuronal fate.