Molecular cloning of cDNA encoding adipogenesis inhibitory factor and identity with interleukin-11

A cDNA encoding a novel adipogenesis inhibitory factor (AGIF) that inhibits the process of adipogenesis in mouse 3T3-L1 preadipocytes was cloned from a cDNA library of the human bone marrow-derived stromal cell line KM-102. The cloned cDNA contains an open reading frame coding for an AGIF precursor...

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Veröffentlicht in:	FEBS letters 1991-06, Vol.283 (2), p.199-202
Hauptverfasser:	Kawashima, Ichiro, Ohsumi, Jun, Mita-Honjo, Katsuko, Shimoda-Takano, Kumi, Ishikawa, Hiroko, Sakakibara, Sachiko, Miyadai, Kenji, Takiguchi, Yo
Format:	Artikel
Sprache:	eng
Schlagworte:	Adipogenesis inhibitory factor Adipose Tissue - drug effects Adipose Tissue - enzymology Amino Acid Sequence Analytical, structural and metabolic biochemistry Base Sequence Biological and medical sciences Blotting, Northern Bone Marrow Bone marrow stromal cell cDNA cloning Cell Line Cloning, Molecular DNA - genetics DNA - isolation & purification Fundamental and applied biological sciences. Psychology Gene Library genes Humans Interleukin-11 Interleukin-II Interleukins - genetics Interleukins - pharmacology Lipids Lipoprotein Lipase - antagonists & inhibitors Miscellaneous Molecular Sequence Data Oligonucleotide Probes Other biological molecules Restriction Mapping RNA, Messenger - genetics Transfection
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Zusammenfassung:	A cDNA encoding a novel adipogenesis inhibitory factor (AGIF) that inhibits the process of adipogenesis in mouse 3T3-L1 preadipocytes was cloned from a cDNA library of the human bone marrow-derived stromal cell line KM-102. The cloned cDNA contains an open reading frame coding for an AGIF precursor of 199 amino acids. Analysis of the sequence of this cDNA revealed identity of this factor with a recently reported novel cytokine, designated interleukin-11 (IL-11). AGIF/IL-11 may play an important role in stromal cell-associated hematopoiesis through its regulatory action on adipocyte differentiation in the bone marrow microenvironment.
ISSN:	0014-5793 1873-3468
DOI:	10.1016/0014-5793(91)80587-S