Analysis of the Albumin/α-Fetoprotein/Afamin/Group specific component gene family in the context of zebrafish liver differentiation

Noël, Emily S.; Reis, Mario dos; Arain, Zoya; Ober, Elke A.

doi:10.1016/j.gep.2010.05.002

Cited by 60 publications

(40 citation statements)

References 42 publications

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“…From the homology of these genes/proteins, an ancestral gene is supposed to split into the DBP/Gc and the albumin/aFP/afamin family about 570-880 million years ago (Mya) whereas the second gene duplication occurred around 360-410 Mya at the time of the divergence of amphibians and reptiles. 56,57 In zebrafish only, one gene is found and has Gc rather than albumin characteristics, although it does not have a vitamin D binding cleft as in avian or mammalian DBP. 56 A study of a very large number of animals (n ¼ 130) by Hay and Watson 58 , using binding characteristics of sera, revealed that all bony fish, birds and mammals use a specific 25OHD binding protein for transport of vitamin D and its metabolites whereas cartilaginous fish and amphibia use lipoproteins.…”

Section: Origin Of the Vitamin D Endocrine System In Vertebratesmentioning

confidence: 99%

“…56,57 In zebrafish only, one gene is found and has Gc rather than albumin characteristics, although it does not have a vitamin D binding cleft as in avian or mammalian DBP. 56 A study of a very large number of animals (n ¼ 130) by Hay and Watson 58 , using binding characteristics of sera, revealed that all bony fish, birds and mammals use a specific 25OHD binding protein for transport of vitamin D and its metabolites whereas cartilaginous fish and amphibia use lipoproteins. Later on, gene and protein analysis refined this analysis.…”

Section: Origin Of the Vitamin D Endocrine System In Vertebratesmentioning

confidence: 99%

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Vitamin D: calcium and bone homeostasis during evolution

2014

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Vitamin D 3 is already found early in the evolution of life but essentially as inactive end products of the photochemical reaction of 7-dehydrocholestol with ultraviolet light B. A full vitamin D (refers to vitamin D 2 and D 3 ) endocrine system, characterized by a specific VDR (vitamin D receptor, member of the nuclear receptor family), specific vitamin D metabolizing CYP450 enzymes regulated by calciotropic hormones and a dedicated plasma transport-protein is only found in vertebrates. In the earliest vertebrates (lamprey), vitamin D metabolism and VDR may well have originated from a duplication of a common PRX/VDR ancestor gene as part of a xenobiotic detoxification pathway. The vitamin D endocrine system, however, subsequently became an important regulator of calcium supply for an extensive calcified skeleton. Vitamin D is essential for normal calcium and bone homeostasis as shown by rickets in vitamin D-deficient growing amphibians, reptiles, birds and mammals. From amphibians onward, bone is gradually more dynamic with regulated bone resorption, mainly by combined action of PTH and 1a, (1,25(OH) 2 D 3 ) on the generation and function of multinucleated osteoclasts. Therefore, bone functions as a large internal calcium reservoir, under the control of osteoclasts. Osteocytes also display a remarkable spectrum of activities, including mechanical sensing and regulating mineral homeostasis, but also have an important role in global nutritional and energy homeostasis. Mineralization from reptiles onward is under the control of well-regulated SIBLING proteins and associated enzymes, nearly all under the control of 1,25(OH) 2 D 3 . The vitamin D story thus started as inert molecule but gained an essential role for calcium and bone homeostasis in terrestrial animals to cope with the challenge of higher gravity and calcium-poor environment.

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Section: Origin Of the Vitamin D Endocrine System In Vertebratesmentioning

confidence: 99%

Section: Origin Of the Vitamin D Endocrine System In Vertebratesmentioning

confidence: 99%

Vitamin D: calcium and bone homeostasis during evolution

2014

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“…The AUC of peptide GQYCYELDEK, from a vitronectin precursor protein, was particularly high (0.978). In fact, the mother proteins of four nonglycosylated tryptic peptides, AGP (41)(42)(43)50), afamin precursor (51,52), isoform HMW of kininogen 1 precursor (53), and a vitronectin precursor (35, 54 -57), are well-characterized proteins related to HCC. Most studies have suggested that changes in the glycosylation of proteins are associated with hepatic diseases.…”

Section: Targeted Mass Spectrometric Approach For Biomarker Discoverymentioning

confidence: 99%

Targeted Mass Spectrometric Approach for Biomarker Discovery and Validation with Nonglycosylated Tryptic Peptides from N-linked Glycoproteins in Human Plasma

Lee¹,

Kim²,

Park³

et al. 2011

Molecular & Cellular Proteomics

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A simple mass spectrometric approach for the discovery and validation of biomarkers in human plasma was developed by targeting nonglycosylated tryptic peptides adjacent to glycosylation sites in an N-linked glycoprotein, one of the most important biomarkers for early detection, prognoses, and disease therapies. The discovery and validation of novel biomarkers requires complex sample pretreatment steps, such as depletion of highly abundant proteins, enrichment of desired proteins, or the development of new antibodies. The current study exploited the steric hindrance of glycan units in N-linked glycoproteins, which significantly affects the efficiency of proteolytic digestion if an enzymatically active amino acid is adjacent to the N-linked glycosylation site. Proteolytic digestion then results in quantitatively different peptide products in accordance with the degree of glycosylation. The effect of glycan steric hindrance on tryptic digestion was first demonstrated using alpha-1-acid glycoprotein (AGP) as a model compound versus deglycosylated alpha-1-acid glycoprotein. Second, nonglycosylated tryptic peptide biomarkers, which generally show much higher sensitivity in mass spectrometric analyses than their glycosylated counterparts, were quantified in human hepatocellular carcinoma plasma using a label-free method with no need for N-linked glycoprotein enrichment. Finally, the method was validated using a multiple reaction monitoring analysis, demonstrating that the newly discovered nonglycosylated tryptic peptide targets were present at different levels in normal and hepatocellular carcinoma plasmas. The area under the receiver operating characteristic curve generated through analyses of nonglycosylated tryptic peptide from vitronectin precursor protein was 0.978, the highest observed in a group of patients with hepatocellular carcinoma. This work provides a targeted means of discovering and validating nonglycosylated tryptic peptides as biomarkers in human plasma, without

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“…40,[54][55][56][57][58][59] This likely reflects the secretory pathway dysfunction that causes a decrease in protein secretion by hepatocytes in patients with liver disease. 47,60 To assess whether hepatocyte protein secretion was impaired by EtOH or Tm exposure, we used a transgenic line in which the vitamin D binding protein (DBP, also called group specific component (gc)), 31,61 the albumin equivalent and major serum protein secreted by fish hepatocytes, 61 is fused to EGFP and expressed under the hepatocyte specific fabp10 promoter Tg(-3.5fabp10a:gc-EGFP) lri500 . This line was crossed to Tg(kdrl:HsHRAS-mCherry) s896 fish in which mCherry is fused to the prenylation sequence in human HRAS, thereby directing it to the membrane of endothelial cells.…”

Section: Fig 2 Tunicamycin and Ethanol Induce Hepatic Dysfunction (A)mentioning

confidence: 99%

Defining Hepatic Dysfunction Parameters in Two Models of Fatty Liver Disease in Zebrafish Larvae

et al. 2013

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Fatty liver disease in humans can progress from steatosis to hepatocellular injury, fibrosis, cirrhosis, and liver failure. We developed a series of straightforward assays to determine whether zebrafish larvae with either tunicamycin-or ethanol-induced steatosis develop hepatic dysfunction. We found altered expression of genes involved in acute phase response and hepatic function, and impaired hepatocyte secretion and disruption of canaliculi in both models, but glycogen deficiency in hepatocytes and dilation of hepatic vasculature occurred only in ethanol-treated larvae. Hepatic stellate cells (HSCs) become activated during liver injury and HSC numbers increased in both models. Whether the excess lipids in hepatocytes are a direct cause of hepatocyte dysfunction in fatty liver disease has not been defined. We prevented ethanol-induced steatosis by blocking activation of the sterol response element binding proteins (Srebps) using gonzo mbtps1 mutants and scap morphants and found that hepatocyte dysfunction persisted even in the absence of lipid accumulation. This suggests that lipotoxicity is not the primary cause of hepatic injury in these models of fatty liver disease. This study provides a panel of parameters to assess liver disease that can be easily applied to zebrafish mutants, transgenics, and for drug screening in which liver function is an important consideration.

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Analysis of the Albumin/α-Fetoprotein/Afamin/Group specific component gene family in the context of zebrafish liver differentiation

Cited by 60 publications

References 42 publications

Vitamin D: calcium and bone homeostasis during evolution

Vitamin D: calcium and bone homeostasis during evolution

Targeted Mass Spectrometric Approach for Biomarker Discovery and Validation with Nonglycosylated Tryptic Peptides from N-linked Glycoproteins in Human Plasma

Defining Hepatic Dysfunction Parameters in Two Models of Fatty Liver Disease in Zebrafish Larvae

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