Cloning of a New "Finger" Protein Gene (ZNF173) within the Class I Region of the Human MHC

Chu, Thomas; Capossela, Angela; Coleman, Roger; Goei, Vita Lan-Ing; Nallur, Girish; Gruen, Jeffrey R.

doi:10.1006/geno.1995.1236

Cited by 55 publications

(22 citation statements)

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“…5), based on the region of homology between RAG-1, Fim B and Fim E, illustrates this relationship. RAG-1 shows homology to eukaryotic proteins involved in such processes as excision repair (yeast RAD16 (64)) and regulation of gene expression (mouse r~t -l r (~~) and to a human acid finger protein (66)). Interestingly, in the phylogenetic tree, RAG-1 clusters closer to the bacterial proteins than it does to any of these eukaryotic proteins (Fig.…”

Section: (3) Conserved Proteins Involved In Vertebrate Adaptive Immunitymentioning

confidence: 99%

Molecular evolution of the vertebrate immune system

Hughes

Yeager

1997

BioEssays

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Adaptive immunity is unique to the vertebrates, and the molecules involved (including immunoglobulins, T cell receptors and the major histocompatibility complex molecules) seem to have diversified very rapidly early in vertebrate history. Reconstruction of gene phylogenies has yielded insights into the evolutionary origin of a number of molecular systems, including the complement system and the major histocompatibility complex (MHC). These analyses have indicated that the C5 component of complement arose by gene duplication prior to the divergence of C3 and C4, which suggests that the alternative complement pathway was the first to evolve. In the case of the MHC, phylogenetic analysis supports the hypothesis that MHC class II molecules evolved before class I molecules. The fact that the MHC-linked proteasome components that specifically produce peptides for presentation by class I MHC appear to have originated before the separation of jawed and jawless vertebrates suggests that the MHC itself may have been present at this time. Immune system gene families have evolved by gene duplication, interlocus recombination and (in some cases) positive Darwinian selection favoring diversity at the amino acid level.

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Section: (3) Conserved Proteins Involved In Vertebrate Adaptive Immunitymentioning

confidence: 99%

Molecular evolution of the vertebrate immune system

Hughes

Yeager

1997

BioEssays

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“…The B-box is then followed by a coiled-coil domain and a variable C-terminal region. RBCC proteins containing a single B-box include RFP (4), TERF (5), SS-A/RO (6), rpt-1 (7), AFP (8), BERP (9), and HERF1 (10).…”

mentioning

confidence: 99%

A Novel RING Finger-B Box-Coiled-Coil Protein, GERP

Vincent

Kwasnicka

Fretier

2000

Biochemical and Biophysical Research Communications

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“…From analysis of 1,974 SNPs for finding association with SLE, 12 SNPs included in this investigation have been found to be associated with SLE (18). Although SLE and AERD occur in different sites of the human body, TRIM26 has been found to be expressed in various tissues including lung tissue (12). In line with this, although mechanisms of AERD are not fully understood, respiratory inflammation by eosinophil infiltration in airway tissues has been regarded as one of the causes of AERD.…”

Section: Discussionmentioning

confidence: 96%

“…In line with this, the protein motifs used in protein-protein interactions and DNA-binding activity are remarkable. The tripartite motif-containing 26 (TRIM26) contains three zinc-binding domains, RING, B-box type 1 and B-box type 2, and a coiled-coil region (12). Although the exact function of TRIM26 still remains unknown, the protein may function in DNA binding through its motifs.…”

Section: Introductionmentioning

confidence: 99%

Association study between TRIM26 polymorphisms and risk of aspirin-exacerbated respiratory disease

Shin¹

2012

Int J Mol Med

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Abstract. Aspirin-exacerbated respiratory disease (AERD) is a clinical syndrome that is characterized by nasal polyposis, general symptoms of asthma and sensitive response to nonsteroidal anti-inflammatory drugs (NSAIDs). Although the exact function of tripartite motif-containing 26 (TRIM26) still remains unknown, the gene functions in the immune response. Thus, we hypothesized that TRIM26 polymorphisms may affect aspirin-induced bronchospasm and explored whether the gene can be a marker for diagnosis of AERD. To investigate our hypothesis that TRIM26 may serve as a genetic marker for diagnosis of AERD, this study focused on demonstrating the associations between single nucleotide polymorphisms (SNPs) of the TRIM26 gene and AERD. We genotyped 18 polymorphisms of TRIM26 in a total of 189 asthmatics and examined their associations with the risk of AERD. We performed logistic analysis for obtaining P-values and regression analysis for demonstrating an association between the phenotype with FEV 1 and the genotype. We observed no associations between polymorphisms in TRIM26 and the risk of AERD in both logistic and regression analyses. Although our results reveal a lack of association, the suggested functional role of TRIM26 makes it a putative candidate gene for AERD. Thus, replications in other populations using larger samples may provide valuable information for AERD etiology.

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Cloning of a New "Finger" Protein Gene (ZNF173) within the Class I Region of the Human MHC

Cited by 55 publications

References 0 publications

Molecular evolution of the vertebrate immune system

Molecular evolution of the vertebrate immune system

A Novel RING Finger-B Box-Coiled-Coil Protein, GERP

Association study between TRIM26 polymorphisms and risk of aspirin-exacerbated respiratory disease

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