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Literature summary for 1.1.1.62 extracted from

  • Strugala, A.J.; Jagodzinski, P.P.
    Conversion of estrone to 17 beta-estradiol in Jurkat acute T cell leukemia Hut-78 T- and Raji B lymphoma cell lines in vitro (2013), Biomed. Pharmacother., 67, 299-303.
    View publication on PubMed

Cloned(Commentary)

Cloned (Comment) Organism
reverse transcription and real-time quantitative PCR expression analysis Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
17beta-estradiol + NAD(P)+ Homo sapiens
-
estrone + NAD(P)H + H+
-
r

Organism

Organism UniProt Comment Textmining
Homo sapiens P14061
-
-

Source Tissue

Source Tissue Comment Organism Textmining
HUT-78 cell a T-lymphoma cell line Homo sapiens
-
JURKAT cell Jurkat acute T cell leukemia cell line Homo sapiens
-
RAJI cell a B-lymphoma cell line Homo sapiens
-
T-47D cell
-
Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
17beta-estradiol + NAD(P)+
-
Homo sapiens estrone + NAD(P)H + H+
-
r

Synonyms

Synonyms Comment Organism
HSD17B1
-
Homo sapiens

Cofactor

Cofactor Comment Organism Structure
NAD+
-
Homo sapiens
NADH
-
Homo sapiens
NADP+
-
Homo sapiens
NADPH
-
Homo sapiens

Expression

Organism Comment Expression
Homo sapiens elevated levels of 17beta-estradiol occur in male patients with chronic lymphocytic leukemia up

General Information

General Information Comment Organism
physiological function endogenous production of 17beta-estradiol in hematological malignant cells might also contribute to immunohormonal imbalance in patients with these disorders. Human T and B lymphocytes are positive for ERa, ERb and GPR30 receptors. Using putative membrane receptors, estrogens are able to modulate cytokine profiles in T cells and the control of B-cell maturation and selection. In particular, estrogens are able to inhibit T cell proliferation, interleukin-2 (IL-2) biosynthesis, and increase B-cell proliferation and antibody production. 17beta-Estradiol is able to upregulate cyclic AMP response element modulator alpha leading to reduced IL-2 gene expression in human T lymphocytes. HSD17B1 may play a crucial role in the development of estrogen-dependent diseases Homo sapiens