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Short-chain dehydrogenases/reductases (SDRs), such as DHRS3, catalyze the oxidation/reduction of a wide range of substrates, including retinoids and steroids (Haeseleer and Palczewski, 2000 [PubMed 10800688]).[supplied by OMIM, Jun 2009].. 再加上，我们可以发Dehydrogenase/reductase (SDR Family) Member 3 蛋白 (4) 和 和数多这个蛋白质的别的产品。
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Human Polyclonal DHRS3 Primary Antibody for ICC, IF - ABIN4305162
Deisenroth, Itahana, Tollini, Jin, Zhang: p53-Inducible DHRS3 is an endoplasmic reticulum protein associated with lipid droplet accumulation. in The Journal of biological chemistry 2011
Human Polyclonal DHRS3 Primary Antibody for WB - ABIN6139597
Zhang, Wang, Cui, Deng, Xu, Yu, Cichello, Serrero, Ying, Liu: Morphologically and Functionally Distinct Lipid Droplet Subpopulations. in Scientific reports 2018
dhrs3 participates in atRA metabolism by reducing atRAL levels and is required for proper anteroposterior axis formation, neuroectoderm patterning, and somitogenesis.
Data show that dhrs3 was activated at the onset of gastrulation, and remained highly expressed at later stages of embryonic development.
Dhrs3a is thus an retinoic acid (RA)-induced feedback inhibitor of RA biosynthesis.
Yap targets Dhrs3, to reduce retinoic acid synthesis and inhibit cardiac fibroblast differentiation during development.
DHRS3 is important in limiting the formation of retinoic acid to ensure the proper development of the coronary vasculature.
Reduction of retinaldehyde by DHRS3 is critical for preventing formation of excess ATRA during embryonic development.
p53-Inducible DHRS3 is an endoplasmic reticulum protein associated with lipid droplet accumulation.
Mouse Dhrs3 plays critical roles in the development of the heart by controlling the formation of retinoic acid.
The retinaldehyde reductase DHRS3 is essential for preventing the formation of excess retinoic acid during mouse embryonic development
we proposed that four newly identified peripheral blood mononuclear cells-derived genes( DHRS3, TTC38, SAP30BP and LPIN2 )could be integrated with previously reported rheumatoid arthritis (RA)-associated genes to monitor and/or diagnose RA.
the bifunctional nature of retinoid oxidoreductase complex provides the RA-based signaling system with robustness by safeguarding appropriate RA concentration despite naturally occurring fluctuations in RDH10 and DHRS3.
Data indicate that retinaldehyde reductase (DHRS3) requires retinol dehydrogenase 10 (RDH10) for full enzymatic activity and, in turn, activates RDH10.
The retSDR1 is identified as novel transcriptional target of the p53 family and not transactivated by EEC syndrome-specific mutations of TAp63gamma.
CST6, CXCL14, DHRS3, and SPP1 are regulated by BRAF signaling and may play a role in papillary thyroid carcinoma pathogenesis
Short-chain dehydrogenases/reductases (SDRs), such as DHRS3, catalyze the oxidation/reduction of a wide range of substrates, including retinoids and steroids (Haeseleer and Palczewski, 2000
retinal dehydrogenase/reductase family member 3
, short-chain dehydrogenase/reductase 3
, dehydrogenase/reductase 3
, dehydrogenase/reductase (SDR family) member 3
, retinal short-chain dehydrogenase/reductase 1
, short chain dehydrogenase/reductase family 16C, member 1
, short-chain dehydrogenase/reductase 1
, dehydrogenase/reductase (SDR family) member 3b