TNFAIP3 interacting protein 3 antibody
- Known as:
- TNFAIP3 interacting protein 3 (anti-)
- Catalog number:
- orb100196
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- TNFAIP3 interacting protein 3 antibody
Related genes to: TNFAIP3 interacting protein 3 antibody
- Gene:
- TNFAIP3 NIH gene
- Name:
- TNF alpha induced protein 3
- Previous symbol:
- -
- Synonyms:
- A20, OTUD7C
- Chromosome:
- 6q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-20
- Date modifiied:
- 2016-10-05
Related products to: TNFAIP3 interacting protein 3 antibody
Related articles to: TNFAIP3 interacting protein 3 antibody
- Ankylosing Spondylitis (AS) is a chronic inflammatory autoimmune rheumatic disease that primarily affects the spine and sacroiliac joints. This study aimed to investigate the expression levels of immune response-related genes, including , , , , , , and , as well as the serum levels of CXCL10 and SIRPA proteins in patients with AS. In addition, the potential diagnostic performance of these molecular and serum biomarkers in distinguishing patients with AS from healthy controls was evaluated. A total of 45 patients with AS and 44 healthy controls were included in the study. Immune-related gene expression levels were analyzed using RT-PCR. In addition, serum CXCL10 and SIRPA protein levels were evaluated using ELISA. The expression levels of , , , , and were significantly increased in patients with AS compared to healthy controls ( < 0.05). In contrast, no significant differences were detected in the expression levels of and . In the ROC analysis, the highest diagnostic performance was obtained for (AUC = 0.741), (AUC = 0.720), and (AUC = 0.722). Serum CXCL10 and SIRPA levels were not significantly different between the groups. In AS, genes particularly associated with NF-κB and interferon signaling pathways (, , , , and ) were found to be significantly altered, and these genes may serve as potential molecular biomarkers for AS. In contrast, the diagnostic power of serum protein biomarkers is limited. These findings indicate that the potential of these genes as biomarkers for AS pathogenesis should be further supported by advanced studies evaluating their expression levels. - Source: PubMed
Publication date: 2026/06/27
Dogan Sevil CeyhanAgbektas TugbaAtas MertKabak GoncaTas AycaSilig Yavuz - Differentiating concurrent general microbial infection from disease flare in Rheumatoid Arthritis (RA) remains challenging. This study evaluated the diagnostic performance of Presepsin and soluble cluster of differentiation 64 (sCD64), and their association with the tumor necrosis factor-alpha-induced protein 3 (TNFAIP3) rs10499194 polymorphism. This case-control study included 90 participants: 30 normal controls, 30 RA without infection, and 30 RA with infection. Serum Presepsin and sCD64 were measured by ELISA, and gene detection for SNP TNFAIP3 rs10499194 (C>T) was performed using the tetra-primer amplification refractory mutation system polymerase chain reaction. Presepsin and sCD64 levels were significantly elevated in the RA with infection group compared to uninfected RA patients and controls (p<0.001). Presepsin (area under the curve, AUC=0.910) and sCD64 (AUC=0.870) outperformed conventional markers (CRP, ESR) in diagnosing infection. The combined biomarkers yielded an AUC of 0.956. The TNFAIP3 T allele was significantly associated with RA susceptibility (OR=2.87, p=0.028). Furthermore, T allele carriers exhibited a dose-dependent, significant increase in both Presepsin (p=0.005) and sCD64 (p=0.013) levels, particularly during infectious episodes. In conclusion, Presepsin and sCD64 are highly accurate biomarkers for distinguishing infection from RA flares. The TNFAIP3 rs10499194 T allele not only increases RA risk but also amplifies the innate immune response during concurrent infections. - Source: PubMed
Mohammed Fatima HAl-Jameel Dheyaa S AHamzah Ali A - Epidermal barrier (EB) function is too often reduced to the role of a passive, inanimate upper strata of dead corneocytes surrounded by extruded lipids. However, this summary fails to appreciate the lower strata keratinocytes (KCs) which serve as both sensors and effectors of immune signaling and thus contribute a dynamic, responsive nature to EB and maintenance and possible decline. In this context, underpinnings of chronic inflammatory skin diseases, e.g. psoriasis and atopic dermatitis, can be better recognized as a feed forward loop in which barrier dysfunction and runaway inflammatory signaling reinforce one another. Traditional therapies addressing these diseases focus on quelling effects and activities of pro-inflammatory extracellular cytokines and their cognate receptors. This paradigm overlooks the promising alternative of augmenting endogenous negative regulators of inflammatory signaling, e.g. the proteins A20 (TNFAIP3) and TNIP1 (ABIN-1) which we propose act as "guardians" restricting NF-κB-dependent inflammatory pathways. Here, we explore the rationale and possible means for targeting these regulators to protect or restore EB integrity. Bolstering these intrinsic quenchers of inflammatory signal progression may offer a path to restore tissue homeostasis and repair the EB in chronic inflammatory disease states. - Source: PubMed
Publication date: 2026/06/30
Samulevich Michael LCarman Liam EAneskievich Brian J - Genetically modified pigs are being developed to address the critical shortage of human organs for transplantation. Although porcine xenografts lacking the three major carbohydrate xenoantigens (3KO) have been considered ideal for human transplantation, the optimal combination of human transgenes (HTGs) to mitigate protein incompatibility remains undefined. In the current study, we evaluate immune responses and transplant outcomes of 3KO kidney xenografts with four different combinations of HTGs in a nonhuman primate model. Here, we show that the addition of HTGs significantly reduces transcripts associated with early immune activation, resulting in markedly prolonged survival of 3KO xenografts. Notably, the inclusion of the anti-inflammatory genes TNFAIP3 and HMOX1 is associated with improved graft survival, significantly reduced T-cell and CD11b⁺ myeloid cell infiltration, and lower expression of rejection-related gene sets in protocol xenograft biopsies. - Source: PubMed
Publication date: 2026/06/27
Karadagi AhmadHirose TakayukiLassiter GraceRosales IvyMa DavidTomosugi ToshihideOtsuka RyoAnand Ranjith PLayer Jacob VChen Jia-YunSantagata SandroCurtis MichaelLow SusanQin WenningColvin Robert BKawai Tatsuo - Selective immunoglobulin A deficiency (IgAD) is the most prevalent primary immunodeficiency and frequently coexists with autoimmune diseases (ADs), suggesting a shared genetic etiology. While genome-wide association studies (GWAS) have identified only a few risk loci for IgAD and hundreds for ADs, systematic cross-trait analyses are lacking, leaving the shared genetic architecture and underlying mechanisms poorly understood. In this study, we analyzed summary statistics from large-scale GWAS of IgAD and 10 common ADs. Cross-trait GWAS meta-analysis identified 51 pleiotropic loci significantly associated with IgAD and at least one AD (p < 5×10⁻⁸), 31 of which were novel for IgAD. Colocalization analysis further supported 33 shared loci between IgAD and ADs, including 19 novel IgAD loci, such as those near TNFAIP3, CD28, IRF4, STAT4, SH2B3, APOBR and RAD51B. Gene-level analysis revealed shared pathways involved in T-cell differentiation and the intestinal immune network for IgA production. Tissue heritability analysis identified whole blood and the intestine as critical tissues, while single-cell RNA sequencing (scRNA-seq) highlighted B cell subtypes in the peripheral blood and gut as the most affected cell types in IgAD and ADs. Mendelian randomization further demonstrated bidirectional causal relationships between IgAD and several ADs. Our findings reveal a shared genetic architecture between IgAD and ADs, highlighting common functional mechanisms and providing insights into their biological interplay and potential immune-based therapies. - Source: PubMed
Publication date: 2026/06/22
Dang XiaoWang Frank QingyunZhang CaicaiSu HuidongLei YaoYang JingLau Yu LungYang Wanling