フェチュイン
- 関
- AFP、alpha-fetoprotein、fetoprotein
WordNet
- any of several antigens that occur naturally in the fetus and sometimes in adults with cancer (同)foetoprotein
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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/06/02 07:19:31」(JST)
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X-ray picture of a Fetuin-A knockout mouse (-/-) compared to a wildtype mouse (+/+). The bright dots in the fetuin-A deficient mouse indicate calcified lesions throughout the body.
Fetuins are blood proteins that are made in the liver and secreted into the bloodstream. They belong to a large group of binding proteins mediating the transport and availability of a wide variety of cargo substances in the bloodstream. The best known representative of these carrier proteins is serum albumin, the most abundant protein in the blood plasma of adult animals. Fetuin is more abundant in fetal blood, hence the name "fetuin" (from Latin, fetus). Fetal calf serum contains more fetuin than albumin, while adult serum contains more albumin than fetuin.
Contents
- 1 Family members
- 2 Animal studies
- 3 Human studies
- 4 References
- 5 Further reading
Family members
Human fetuin is synonymous with α2-HS-glycoprotein (genetic symbol AHSG), α2-HS, A2HS, AHS, HSGA, and fetuin-A. Fetuin-A exists as a single-copy gene in the human and mouse genomes. A closely related gene, fetuin-B, also exists in the human, rat, and mouse genomes. Like fetuin-A, fetuin-B is made predominantly by the liver and to a lesser extent by a number of secretory tissues. Fetuins exist in all vertebrate genomes including fish and reptiles. Fetuins are members of a family of proteins that evolved from the protein cystatin by gene duplication and exchange of gene segments. Fetuins thus belong to the cystatin superfamily of proteins. Fetuin relatives within this superfamily are the histidine-rich glycoprotein (HRG) and kininogen (KNG).
Α2-HS-glycoprotein |
Identifiers |
Symbol |
AHSG |
Alt. symbols |
FETUA, A2HS, HSGA |
Entrez |
197 |
HUGO |
349 |
OMIM |
138680 |
RefSeq |
NM_001622 |
UniProt |
P02765 |
Other data |
Locus |
Chr. 3 q27.3 |
|
fetuin-B |
Identifiers |
Symbol |
FETUB |
Alt. symbols |
16G2, Gugu |
Entrez |
26998 |
HUGO |
3658 |
OMIM |
605954 |
RefSeq |
NM_014375 |
UniProt |
Q9UGM5 |
Other data |
Locus |
Chr. 3 q27.3 |
|
Animal studies
The function of Fetuin-A in the body was determined by gene knockout technology in mice. Knocking out the gene for fetuin-A rendered the mice completely fetuin-A deficient. Feeding a mineral-rich diet to fetuin-A-deficient mice resulted in widespread calcification (ectopic mineralization) of lung, heart, and kidneys in these mice. The calcification became drastically exacerbated when the fetuin-A knockout was combined with the genetic background DBA/2. The mouse strain DBA/2 is known for its proneness to calcify damaged tissues, a process called "dystrophic calcification". Fetuin-A deficiency dramatically increased the calcification proneness of these mice in that all mice sponteneously calcified throughout their body even without a mineral-rich diet or surgical tissue trauma. Fetuin-A is therefore regarded as a potent inhibitor of systemic calcification.
Human studies
Fetuin-A was originally discovered to be an inhibitor of vascular calcification in early 1990s. Since then the biologic roles attributed to fetuin-A has increased exponentially. Fetuin-A has been demonstrated to play an important role in free fatty acid induced insulin resistance at liver. Increased fetuin-A in patients with pre-diabetes is associated with increased progression to diabetes and decreased reversal to normoglycemia. Hence fetuin-A is a predictor of adverse glycemic outcomes in pre-diabetes.[1][unreliable medical source] Increased fetuin-A had been also been linked to increased occurrence of non-alcoholic fatty liver disease and cardiovascular events, believed to be due to its proinflammatory effects. Fetuin-A in contrast has also been demonstrated to have anti-inflammatory properties. It is a negative acute-phase reactant in sepsis and endotoxemia, promotes wound healing, and is neuroprotective in Alzheimer's disease. Decreased fetuin-A is a predictor of increased disease activity in obstructive lung disease, Crohn's disease, and ulcerative colitis. Differential effects on different toll like receptors in different tissues and organ systems may explain this pradoxical effects in different systems.[2][unreliable medical source]
References
- ^ Dutta D, Mondal SA, Kumar M, Hasanoor Reza AH, Biswas D, Singh P et al. (2014). "Serum fetuin-A concentration predicts glycaemic outcomes in people with prediabetes: a prospective study from eastern India". Diabet. Med. 31 (12): 1594–9. doi:10.1111/dme.12539. PMID 24975463.
- ^ Mukhopadhyay S, Mondal SA, Kumar M, Dutta D (2014). "Proinflammatory and antiinflammatory attributes of fetuin-a: a novel hepatokine modulating cardiovascular and glycemic outcomes in metabolic syndrome". Endocr Pract 20 (12): 1345–51. doi:10.4158/EP14421.RA. PMID 25370330.
Further reading
- Demetriou M, Binkert C, Sukhu B, Tenenbaum HC, Dennis JW (1996). "Fetuin/alpha2-HS glycoprotein is a transforming growth factor-beta type II receptor mimic and cytokine antagonist". J. Biol. Chem. 271 (22): 12755–61. doi:10.1074/jbc.271.22.12755. PMID 8662721.
- Jahnen-Dechent W, Schäfer C, Ketteler M, McKee MD (2008). "Mineral chaperones: a role for fetuin-A and osteopontin in the inhibition and regression of pathologic calcification". J. Mol. Med. 86 (4): 379–89. doi:10.1007/s00109-007-0294-y. PMID 18080808.
- Schafer C, Heiss A, Schwarz A, Westenfeld R, Ketteler M, Floege J et al. (2003). "The serum protein alpha 2-Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification". J. Clin. Invest. 112 (3): 357–66. doi:10.1172/JCI17202. PMC 166290. PMID 12897203.
- Ketteler M, Bongartz P, Westenfeld R, Wildberger JE, Mahnken AH, Böhm R et al. (2003). "Association of low fetuin-A (AHSG) concentrations in serum with cardiovascular mortality in patients on dialysis: a cross-sectional study". Lancet 361 (9360): 827–33. doi:10.1016/S0140-6736(03)12710-9. PMID 12642050.
- Heiss A, DuChesne A, Denecke B, Grötzinger J, Yamamoto K, Renné T et al. (2003). "Structural basis of calcification inhibition by alpha 2-HS glycoprotein/fetuin-A. Formation of colloidal calciprotein particles". J. Biol. Chem. 278 (15): 13333–41. doi:10.1074/jbc.M210868200. PMID 12556469.
UpToDate Contents
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English Journal
- Mammalian Sialyltransferase ST3Gal-II: Its Exchange Sialylation Catalytic Properties Allow Labeling of Sialyl Residues in Mucin-Type Sialylated Glycoproteins and Specific Gangliosides.
- Chandrasekaran EV, Xue J, Xia J, Locke RD, Patil SA, Neelamegham S, Matta KL.SourceDepartment of Cancer Biology, Roswell Park Cancer Institute , Buffalo, New York 14263, United States.
- Biochemistry.Biochemistry.2011 Nov 8;50(44):9475-87. Epub 2011 Oct 13.
- While glycosyltransferases are known to display unidirectional enzymatic activity, recent studies suggest that some can also catalyze readily reversible reactions. Recently, we found that mammalian sialyltransferase ST3Gal-II can catalyze the formation of CMP-NeuAc from 5'-CMP in the presence of a d
- PMID 21913655
- Effects of Pioglitazone versus Simvastatin on Biomarkers of Inflammation in Patients on High Cardiovascular Risk.
- Hanefeld M, Schaper F, Appelt D, Fuchs W.AbstractHigh levels of fetuin-A has been linked to cardiovascular disease, possibly via modulating low-grade systemic inflammation. We performed a subanalysis from the PIOSTAT study to investigate a possible link between fetuin-A and the inflammatory biomarker hs-CRP. 66 nondiabetic individuals at cardiovascular risk were randomized to either pioglitazone, simvastatin, or the combination of both, and followed for 12 weeks. At study endpoint, correlations between serum fetuin-A, hs-CRP, blood lipids, PAI-1, MMP-9, HOMA-IR, and liver transaminases were investigated by Spearman rank correlation. Changes in fetuin-A concentration did not correlate to changes in hs-CRP (r=0.19, p=0.16). A positive correlation was found for change of HOMA-IR value (r=0.33, p=0.01) and for the AST/ALT ratio (p<0.05). Our data suggest that the previously observed correlation between elevated circulating fetuin-A and hs-CRP in epidemiological studies may not reflect a causal relationship in nondiabetic patients on high cardiovascular risk.
- Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme.Horm Metab Res.2011 Nov 8. [Epub ahead of print]
- High levels of fetuin-A has been linked to cardiovascular disease, possibly via modulating low-grade systemic inflammation. We performed a subanalysis from the PIOSTAT study to investigate a possible link between fetuin-A and the inflammatory biomarker hs-CRP. 66 nondiabetic individuals at cardiovas
- PMID 22068809
Japanese Journal
- 血液透析患者における Fetuin-A 濃度の低値は頸動脈石灰化および内中膜肥厚の進展に関与していた
- 對馬 惠,蔦谷 知佳子,寺山 百合子,山谷 金光,今井 篤,齋藤 久夫,舟生 富寿
- 日本透析医学会雑誌 = Journal of Japanese Society for Dialysis Therapy 43(5), 443-452, 2010-05-28
- … 管石灰化は動脈硬化を重症化させる深刻な問題である.Fetuin-A(alpha 2-Heremans-Schmid glycoprotein)は血管石灰化を抑制する作用を有し,透析患者においては栄養障害・炎症とも関与していることから,動脈硬化関連因子でもある.われわれは,血液透析患者に対し頸動脈エコーを経時的に施行し,動脈硬化の程度(石灰化および内中膜肥厚)とFetuin-A濃度との関連性について検討した.対象78例の平均年 …
- NAID 10026420773
- Toxic isolectins from the mushroom Boletus venenatus.
- Horibe Masashi,Kobayashi Yuka,Dohra Hideo,Morita Tatsuya,Murata Takeomi,Usui Taichi,Nakamura-Tsuruta Sachiko,Kamei Masugu,Hirabayashi Jun,Matsuura Masanori,Yamada Mina,Saikawa Yoko,Hashimoto Kimiko,Nakata Masaya,Kawagishi Hirokazu
- Phytochemistry 71(5-6), 648-657, 2010-04
- … Among the glycoproteins examined, asialo-fetuin was the strongest inhibitor. …
- NAID 120002227905
Related Links
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- Animal studies [edit] The function of Fetuin-A in the body was determined by gene knockout technology in mice. Knocking out the gene for fetuin-A rendered the mice completely fetuin-A deficient. Feeding a mineral-rich diet to fetuin ...
- フェチュインA(Fetuin A)は,飽和脂肪酸によるインスリン抵抗性を促進するTLR4の内因性リガンドとして作用します。TLR4は炎症性シグナル経路を活性化させ,先天的な免疫に関し重要な役割を果たしています。遊離脂肪酸はTLR4経路を ...
Related Pictures
★リンクテーブル★
[★]
フェトプロテイン、胎児タンパク質、胎児蛋白
- 関
- AFP、alpha-fetoprotein、fetal protein、fetuin
[★]
- 英
- fetuin
- 関
- フェトプロテイン、αフェトプロテイン、α-フェトプロテイン