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1 RALDH 1 immunoreactivity was localized to sustentacular
2 RALDH 1, 2, and 3 mRNAs were detected in postnatal rat o
3 RALDH 2 did not colocalize with RALDH 1, but appeared to
4 RALDH activity was up-regulated in all 3 populations of
5 RALDH mutant mice also have reduced contractility in the
6 RALDH-2 and CYP26, two key enzymes that carry out retino
7 RALDH-2-IR indicates dynamic and discrete patterns of re
12 LP (differentially catalyzed by RALDH 1 and RALDH 2) at sites that could influence the development,
13 zed to RALDH 1(+) sites in the OE and LP and RALDH 2(+) sites, primarily surrounding nerve fiber bund
14 -beta and retinal dehydrogenases (RALDH1 and RALDH 2) under steady-state conditions and that their sa
16 d underlying LP (differentially catalyzed by RALDH 1 and RALDH 2) at sites that could influence the d
17 ynthesized in the postnatal OE (catalyzed by RALDH 1) and underlying LP (differentially catalyzed by
20 RA-synthesizing retinaldehyde dehydrogenase RALDH-2, is likely to represent a diffusion source of RA
22 lerance by expressing retinal dehydrogenase (RALDH), an enzyme that promotes retinoic acid, which aid
23 in C57Bl/6 and retinaldehyde dehydrogenase (RALDH) 1 knockout (KO) mice fed a high-fat (HF) diet.
25 s the synthetic retinaldehyde dehydrogenase (RALDH) enzymes and it is currently thought that switchin
26 f cytokines and retinaldehyde dehydrogenase (RALDH) enzymes in ileum samples, DCs, and IECs by real-t
27 fy and localize retinaldehyde dehydrogenase (RALDH) expression in postnatal rat OE to gain a better u
29 d enzymes, the retinaldehyde dehydrogenases (RALDH), and binds to and activates nuclear RA receptors
31 eport the immunolocalization of this enzyme (RALDH-2-IR) in stage 6-29 chicken embryos; we also show
39 H 1, but appeared to be expressed in GFAP(-)/RALDH 1(-) OECs as well as in unidentified structures in
42 soderm expresses little RALDH-2-IR; however, RALDH-2-IR is strongly expressed in tissues adjacent to
43 first, prepubertal, spermatogenic cycle (i) RALDH-dependent synthesis of RA by Sertoli cells (SC), t
44 repressor, which appears to directly inhibit RALDH expression in DCs, thus providing mechanistic insi
45 of PGE2 during DC differentiation inhibited RALDH expression in mouse and human DCs, abrogating thei
46 he developing limb mesoderm expresses little RALDH-2-IR; however, RALDH-2-IR is strongly expressed in
51 or SREBP-1c downregulated the expression of RALDH genes, which could be rescued by re-expressing SRE
53 ng PGE2 signaling increased the frequency of RALDH(+) DCs in vitro, and reducing PGE2 synthesis in vi
54 eric lymph node DC with the highest level of RALDH activity, and ligation of 4-1BB maintained RALDH e
55 st cells do not express detectable levels of RALDH-2, but migrating crest cells are associated with R
58 imb region, a similar spatial segregation of RALDH-2 and CYP26 expression was found at stages 14 and
59 not expressed by DCs, it was the predominant RALDH enzyme isoform expressed by intestinal CD14(+) mac
62 istochemistry on the embryonic trunk reveals RALDH-2 mRNA both in mesoderm and neuroectoderm, with hi
65 e also show that tissues that exhibit strong RALDH-2-IR in the embryo contain RALDH-2 and synthesize
68 e strong support for CYP1B1 being one of the RALDH-independent components by which embryos direct RA-
69 re expressed in the epithelium overlying the RALDH-3 expressing fibroblasts of the lamina propria.
70 vitro assay, addition of recombinant CRBP to RALDH-2 increased RA synthesis from retinaldehyde, with
71 de binding protein (CRBP I) was localized to RALDH 1(+) sites in the OE and LP and RALDH 2(+) sites,
72 ient mesenteric lymph node DC displayed weak RALDH activity and were poor at promoting iTreg developm
76 re expressed in nonoverlapping regions, with RALDH-2 transcripts localized to the presumptive presomi
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