SERPINA7 Antibody (OASA09278)
- Known as:
- SERPINA7 Antibody (OASA09278)
- Catalog number:
- oasa09278
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SERPINA7 Antibody (OASA09278)
Related genes to: SERPINA7 Antibody (OASA09278)
- Gene:
- SERPINA7 NIH gene
- Name:
- serpin family A member 7
- Previous symbol:
- TBG
- Synonyms:
- -
- Chromosome:
- Xq22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: SERPINA7 Antibody (OASA09278)
Related articles to: SERPINA7 Antibody (OASA09278)
- Asthma is a Th2-skewed inflammatory disorder characterized by eosinophilic infiltration, cytokine dysregulation, and airway remodeling. Emerging evidence highlights the role of immunometabolic pathways and the gut-lung axis in asthma pathogenesis. - Source: PubMed
Publication date: 2026/06/03
Yang HangruiWu GeyuanLiang ShuoZan RaonaChen YitaoYuan WeiweiChen HongHuang Guiqiong - This prospective study evaluated first-trimester markers in pregnancies with isolated and combined forms of fetal growth disorders and gestational diabetes mellitus (GDM). Among 1869 screened women, the analysis included 83 controls, 55 GDM, 22 isolated intrauterine growth restriction (iIUGR), and 33 isolated large-for-gestational-age (iLGA) cases, with GDM subgroups stratified by fetal growth (GDM with normal fetal weight, GDM + IUGR, and GDM + LGA). First-trimester clinical and routine biochemical parameters were recorded, and serum concentrations of 80 proteins were measured using targeted LC-MRM-MS proteomics. Different trajectories emerged: IUGR phenotypes showed low PAPP-A/PlGF and high TSH ( < 0.01), indicating early placental insufficiency, while macrosomia showed opposite trends. GDM + IUGR represented the most severe "double hit" phenotype (lowest PlGF, earliest delivery), whereas GDM + LGA showed increased umbilical artery resistance despite excessive growth, suggesting endothelial dysfunction. Targeted proteomics revealed characteristic signatures: iIUGR featured low complement () and IGF proteins (, ) versus GDM and iLGA ( < 0.001); GDM + IUGR showed elevated and versus iIUGR ( < 0.05); GDM + LGA was marked by high and low , versus iLGA ( < 0.05). Complement and IGF pathways were consistently implicated. Machine learning achieved 77% sensitivity for IUGR prediction using clinical parameters and 88% sensitivity for LGA prediction using proteomic data. These findings demonstrate that fetal growth disorders represent pathophysiologically unique entities detectable in the first trimester, enabling early risk stratification and personalized management. - Source: PubMed
Publication date: 2026/05/08
Starodubtseva NataliaTokareva AlisaFrankevich NataliaKononikhin AlexeyBugrova AnnaIndeykina MariaKukaev EvgeniiDerenko AnnaFrankevich VladimirNikolaev EvgenySukhikh Gennady - Radiation pneumonitis (RP) is a dose-limiting toxicity in lung cancer radiation therapy, often poorly predicted by static clinical and dosimetric models. We aimed to identify a robust, blood-based proteomic signature grounded in the longitudinal biological response to radiation to enable accurate, early risk stratification. - Source: PubMed
Publication date: 2026/05/22
Wu LingyunMasaki NakamuraMukohara ToruYang JingSun ZeyuRen ChunyunChen DeyingJiang KanTang QiuyingDing KaikaiYin XinYu HaoZhou YuzhengWang SiyuanYin JieYan YonghengHe YuLi QuanhaiWei WeiLu ZhongjieSun XiaoliMa ChiyuanYe XianghuaYan Senxiang - BACKGROUND: Inherited Thyroxine-binding globulin (TBG) deficiency is a rare X-linked disorder caused by mutations in the SERPINA7 gene. This study aimed to investigate the underlying molecular defect in a hypothyroid patient undergoing levothyroxine (L-T4) therapy who exhibited persistent discordant thyroid function test (TFT) results and to characterise the structural and functional consequences of the mutation identified. METHODS: Thyroid function tests (TFT) were estimated by immunoassays. Genomic DNA from the proband, her family members, and control subjects was PCR-amplified for SERPINA7 exons using specific primers, followed by Sanger sequencing. Allele-specific PCR was employed to validate the mutation site. Further, Whole-exome sequencing was performed as an orthogonal validation to reconfirm the genomic location and exclude additional variants. In silico tools were used to model the mutant protein’s secondary and tertiary structures to assess potential structural alterations. RESULTS: A complex indel mutation in SERPINA7, annotated as NM_000354.6:c.1117_1118delinsCAG, resulting in NP_000345.2:p.Ser353Glnfs*5, was detected in exon 4 (mature protein numbering). This mutation, referred to as TBG-CD-Ind (GenBank accession no. PV670074), was previously documented in another unrelated family and resulted in a frameshift that introduces a premature stop codon at position 357. Consequently, the translation process was prematurely terminated, leading to the production of a truncated TBG protein. Structural modelling of the mutant TBG predicted significant alterations in its secondary and tertiary structures, providing mechanistic insights into the mutation-induced conformational changes. Superimposition of native and mutant TBG structures indicated gross conformational collapse, indicating likely misfolding, degradation, and secretion failure of the mutant protein. CONCLUSION: In silico structural analysis indicated that TBG-CD-Ind belongs to the list of convoluted mutations reported in the SERPINA7 gene so far. Recurrent identification of the TBG-CD-Ind mutation in unrelated Indian families, together with its absence from global population databases, indicates potential founder effect-driven enrichment and warrants further population-based studies. Its coexistence with hypothyroidism complicated therapeutic decision-making. Awareness of this rare condition is essential to avoid misinterpretation of TFT, inappropriate dose escalation, and suboptimal management, supporting the inclusion of TBG assessment in routine thyroid evaluation. - Source: PubMed
Publication date: 2026/03/25
Gawandi SmitaKhati HarshlataMalhotra GauravBaghel Nawab Singh - A certain population of patients exhibits discordant thyroid function tests (TFT) consistently along with unclear symptoms may lead to equivocal diagnosis and treatment. Concomitant elevation in TSH and T4 is one of the patterns of discordant TFT which can be associated with different thyroid-related conditions and, hence, warrants differential diagnosis. A case of congenital hypothyroidism was investigated to determine the etiology of the consistent co-elevation in TSH and T4 despite thyroxine supplementation since birth. T4 dose was changed multiple times which caused abrupt fluctuations in TSH and T4 levels in the previous treatment. The index patient, II-1 did not have pituitary or liver abnormality or any transient factors that would elevate thyroid hormone-binding proteins. The results revealed that II-1 had TBG-excess. However, no mutation or copy number variation in the gene which codes for TBG was detected. Further, II-1 was detected with a homozygous mutation, c.955G > A in the exon 8 of the gene associated with CH. His mother and siblings were heterozygous for the mutation, however, they had normal TBG and TFT. The present study is the first report of the rare combination of endocrine disorders i.e., TBG-excess and CH, and is also the first report of the mutation c.955G > A from Indian ethnic origin. The co-occurrence of two endocrine abnormalities caused TFT discordance and confusion. This study highlights the importance of detailed biochemical and genetic testing for the differential diagnosis of thyroid disorders in patients exhibiting discrepant TFT results which would avoid misdiagnosis and inappropriate treatment. - Source: PubMed
Publication date: 2024/03/15
Gawandi SmitaKumarasamy JKulkarni Savita