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Merck
모든 사진(1)

문서

SAE0096

Sigma-Aldrich

IDO1, human

recombinant, expressed in E. coli, lyophilized powder, His tagged

동의어(들):

Indoleamine 2,3-dioxygenase 1

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About This Item

효소 위원회 번호:
UNSPSC 코드:
12352202
NACRES:
NA.26

재조합

expressed in E. coli

형태

lyophilized powder

특이 활성도

800 units/μg

UniProt 수납 번호

배송 상태

wet ice

저장 온도

−20°C

일반 설명

IDO1 is a heme-enzyme that is induced by INF-γ and catalyzes the conversion of tryptophan to kynurenine. This leads to a depletion of tryptophan that results in T cells and dendritic cells inactivation. IDO activity has been identified as an important immune effector pathway in tumor cells to escape a potentially effective immune response. Inhibition of IDO1 has been found to delay cancer growth and enhance dendritic vaccines. Therapeutic inhibition of IDO1 is of interest because of its proposed role in the pathogenesis of several diseases, including cancer, hypotension, neurodegenerative disorders, and its potential to aid cancer immunotherapy and organ transplant.
This recombinant human IDO1 has a 6x histidine tag at its N-terminus. This product is lyophilized from a solution containing 10 mM Trizma buffer (pH 7.0), with 500 mM NaCl and a carbohydrate carrier.

단위 정의

One unit of enzyme hydrolyzes 1.0 pmole of L-Tryptophan to N-formyl-Lkynurenine per minute at pH-6.5 at 37°C

Storage Class Code

11 - Combustible Solids

WGK

WGK 2

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


시험 성적서(COA)

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문서 라이브러리 방문

Immune-modulating enzyme indoleamine 2,3-dioxygenase is effectively inhibited by targeting its apo-form
Nelp, M.T. et al.
Proceedings of the National Academy of Sciences of the USA, 115(13), 3249-3254 (2018)
Indoleamine 2,3-dioxygenase: is it an immune suppressor?
Sollman, H. et al.
Cancer Journal, 16(4), 354-359 (2010)
Human bone marrow stromal cells inhibit allogeneic T-cell responses by indoleamine 2,3-dioxygenase-mediated tryptophan degradation.
Meisel, R. et al.
Blood, 103(12), 4619-4621 (2004)
Ji-Hee Shin et al.
European journal of nutrition, 59(8), 3591-3601 (2020-02-15)
Growing evidence shows that nutrient metabolism affects inflammatory bowel diseases (IBD) development. Previously, we showed that deficiency of indoleamine 2,3-dioxygenase 1 (Ido1), a tryptophan-catabolizing enzyme, reduced the severity of dextran sulfate sodium (DSS)-induced colitis in mice. However, the roles played

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