1 g ET-2 at Trp(21)-Val(22), yielding ET-1 and
ET-2.
2 ASO designs comprised of short S-cEt (S-2'-O-
Et-2',
4'-bridged nucleic acid) gapmer ASOs, approximatel
3 ncreased resting IMTG content (SIT 1.7-fold,
ET 2.
4-fold; P < 0.05), concomitant with parallel increa
4 h parallel increases in PLIN2 (SIT 2.3-fold,
ET 2.
8-fold; P < 0.01) and PLIN5 expression (SIT 2.2-fol
5 Incubation of tumor cells with
ET-2 also increased chemotaxis toward the chemokines CXC
6 have studied the role of endothelins (ET-1,
ET-2 and ET-3) and ET receptors (ET-RA and ET-RB) in the
7 ET-2 and ET-7 complex (serotype AD) isolates were recove
8 ulation affects ET isoform expression (ET-1,
ET-2,
and ET-3) through capacitative Ca2+ influx.
9 Its 3 isoforms, ET-1,
ET-2,
and ET-3, mediate several physiologic actions in s
10 lines tested, all expressed mRNAs for ET-1,
ET-2,
and ET-RB.
11 f breast tumor cells, which express ET-1 and
ET-2 as well as ET-RA and ET-RB.
12 lesser extent, also cleaved big ET-1 and big
ET-2 at Trp(21)-Val(22), yielding ET-1 and ET-2.
13 Breast tumor cells migrated toward ET-1 and
ET-2 but not toward ET-3.
14 Finally, systemically inducible
ET-2 deficiency in neonatal and adult mice fully reprodu
15 Identification of ET-1 and
ET-2 gene expression in BCE strengthens the notion that
16 The significant residual ET-1/
ET-2 in the ECE-1(-/-); ECE-2(-/-) embryos indicates tha
17 Levels of mature ET-1 and
ET-2 in whole ECE-1(-/-); ECE-2(-/-) embryos at E12.5 do
18 inducing chemotaxis of tumor cells, ET-1 and
ET-2 increased tumor cell invasion through Matrigel.
19 Although
ET-2 is abundantly expressed in the gastrointestinal tra
20 Together, these findings reveal that
ET-2 is critical for the growth and survival of postnata
21 ET-1,
ET-2 isoforms, and ET receptor mRNAs were identified.
22 the physiological functions of endothelin-2 (
ET-2),
we generated gene-targeted mouse models.