A Constitutively Expressed Serum Amyloid A Protein Gene (SAA4) Is Closely Linked to, and Shares Structural Similarities with, an Acute-Phase Serum Amyloid A Protein Gene (SAA2)

Steel, D. M.; Sellar, Grant C.; Uhlar, Clarissa M.; Simon, Susan; DeBeer, Fred C.; Whitehead, Alexander S.

doi:10.1006/geno.1993.1209

Cited by 57 publications

(51 citation statements)

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“…The SAA proteins may be classified, with respect to their induction profiles, as either acute-phase (A-SAAs) or constitutive (C-SAAs) [4][5][6]. The A-SAA genes of both humans (SAA1, SAA2) and mice (Saa1, Saa2, Saa3) exhibit co-ordinate transcriptional control and a characteristically rapid and dramatic induction during the acute response phase [7,8].…”

Section: Introductionmentioning

confidence: 99%

“…The Saa5 gene was determined to have a 4 exon/3 intron structure, in keeping with the organization of all other described Saa genes [9]. Furthermore, the Saa5 exon/ intron junction positions thus identified were those which would be predicted from a comparison of the mouse SAA5 cDNA sequence to the known gene structures of the mouse A-Saa and human SAA4 genes [4,14]. An analysis of Saa5 intronic sequences is presented in Table 1, in which the size of the three introns, and degree of nucleotide identity to the introns of the constitutive human SAA4 gene, are detailed.…”

Section: Ecorif/msaa5ecorir and Msaa4lf/msaa5lr5mentioning

confidence: 99%

“…In contrast, the C-SAA genes of humans (SAA4) and mice (Saa5) are expressed at comparatively low levels following an inflammatory stimulus [4,6]. Furthermore, human SAA4 and mouse SAA5 proteins have been identified as normal apolipoprotein components of non-acute-phase HDL, while the A-SAA proteins are essentially only expressed under acute-phase conditions [4,6,9].…”

Section: Introductionmentioning

confidence: 99%

“…The A-SAA genes of both humans (SAA1, SAA2) and mice (Saa1, Saa2, Saa3) exhibit co-ordinate transcriptional control and a characteristically rapid and dramatic induction during the acute response phase [7,8]. In contrast, the C-SAA genes of humans (SAA4) and mice (Saa5) are expressed at comparatively low levels following an inflammatory stimulus [4,6]. Furthermore, human SAA4 and mouse SAA5 proteins have been identified as normal apolipoprotein components of non-acute-phase HDL, while the A-SAA proteins are essentially only expressed under acute-phase conditions [4,6,9].…”

Section: Introductionmentioning

confidence: 99%

“…9). The mouse Saa and human SAA genes have been extensively characterized with respect to gene sequences and relative map positions [4,[14][15][16][17][18][19]. It is of considerable interest to further characterize the mouse Saa5 gene, which represents the only identified mouse constitutive Saa gene, and, as such, is a candidate evolutionary homologue of the human SAA4 gene.…”

Section: Introductionmentioning

confidence: 99%

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Structure of the Mouse Serum Amyloid A 5 (Saa5) Gene: Relationship to Other Members of the Serum Amyloid A Family

Butler

Whitehead

1997

Scand J Immunol

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The mouse and human genes which encode the serum amyloid A (SAA) proteins have been extensively characterized. In the present study, the authors report the sequencing of the constitutively expressed mouse Saa5 gene, including ≈2 kilobases of promoter sequence which extends into the sequence of the adjacent Saa4 pseudogene. The Saa5 gene was thus determined to have a 4 exon/3 intron structure, with a B2 repeat located ≈450 base pairs upstream, and a microsatellite contained within intron 2. Analyses of Saa5 intronic and promoter sequences, by comparison with representative members of the mouse Saa and human SAA families, provided evidence which strongly suggests that mouse Saa5 and the constitutively expressed human SAA4 gene are evolutionary and functional homologues. Furthermore, putative transcription motifs were identified within the Saa5 and SAA4 promoters which may account, in part, for the constitutive expression and unique induction profiles of these genes.

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Section: Introductionmentioning

confidence: 99%

Section: Ecorif/msaa5ecorir and Msaa4lf/msaa5lr5mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Structure of the Mouse Serum Amyloid A 5 (Saa5) Gene: Relationship to Other Members of the Serum Amyloid A Family

Butler

Whitehead

1997

Scand J Immunol

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Serum amyloid A1 (SAA1) protein in human colostrum

et al. 2018

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Proteins of the serum amyloid A ( SAA ) family have been remarkably conserved in evolution. Their biologic function(s) are not fully defined but they are likely to be a part of primordial host defense. We have detected a ∼ 12‐kDa protein reacting with antibodies against serum amyloid A ( SAA ) in human colostrum by western blotting. Mass spectrometry identified the reactive species as SAA 1, previously identified as a prominent member of the acute‐phase response in serum. Our finding SAA 1 in human colostrum contrasts with bovine, caprine and ovine colostrum where a species corresponding to putative SAA 3 is uniformly present. SAA 1 protein in human colostrum presumably contributes to neonatal protection.

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Osteocytes/Osteoblasts Produce SAA3 to Regulate Hepatic Metabolism of Cholesterol

Huang,

Jiang,

et al. 2024

Advanced Science

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Hypercholesterolaemia is a systemic metabolic disease, but the role of organs other than liver in cholesterol metabolism is unappreciated. The phenotypic characterization of the Tsc1Dmp1 mice reveal that genetic depletion of tuberous sclerosis complex 1 (TSC1) in osteocytes/osteoblasts (Dmp1‐Cre) triggers progressive increase in serum cholesterol level. The resulting cholesterol metabolic dysregulation is shown to be associated with upregulation and elevation of serum amyloid A3 (SAA3), a lipid metabolism related factor, in the bone and serum respectively. SAA3, elicited from the bone, bound to toll‐like receptor 4 (TLR4) on hepatocytes to phosphorylate c‐Jun, and caused impeded conversion of cholesterol to bile acids via suppression on cholesterol 7 α‐hydroxylase (Cyp7a1) expression. Ablation of Saa3 in Tsc1Dmp1 mice prevented the CYP7A1 reduction in liver and cholesterol elevation in serum. These results expand the understanding of bone function and hepatic regulation of cholesterol metabolism and uncover a potential therapeutic use of pharmacological modulation of SAA3 in hypercholesterolaemia.

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A Constitutively Expressed Serum Amyloid A Protein Gene (SAA4) Is Closely Linked to, and Shares Structural Similarities with, an Acute-Phase Serum Amyloid A Protein Gene (SAA2)

Cited by 57 publications

References 0 publications

Structure of the Mouse Serum Amyloid A 5 (Saa5) Gene: Relationship to Other Members of the Serum Amyloid A Family

Structure of the Mouse Serum Amyloid A 5 (Saa5) Gene: Relationship to Other Members of the Serum Amyloid A Family

Serum amyloid A1 (SAA1) protein in human colostrum

Osteocytes/Osteoblasts Produce SAA3 to Regulate Hepatic Metabolism of Cholesterol

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