CALD ELISA kit
- Known as:
- CALD Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CALD-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CALD ELISA kit
Related genes to: CALD ELISA kit
- Gene:
- RASGRP2 NIH gene
- Name:
- RAS guanyl releasing protein 2
- Previous symbol:
- -
- Synonyms:
- CALDAG-GEFI
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-21
- Date modifiied:
- 2019-04-23
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- Psoriasis is a chronic inflammatory autoimmune skin disease for which no standardised and reliable molecular biomarkers of disease course or activity are currently available. Here, we aimed to identify serum biomarkers of psoriasis. Serum samples from 40 patients with psoriasis and 40 healthy volunteers were analysed using ELISA and Proximity Extension Assay proteomics. ELISA revealed significantly increased serum levels of AGO2 and APOA1 in psoriatic patients versus controls, with a strong association between APOA1 and psoriasis (OR = 20.72, 95% CI of 4.57-93.87, = 0.000137). Targeted serum proteomics additionally identified 35 differentially expressed proteins, including well-known psoriasis drivers (e.g., top upregulated IL17A and SERPINB4). The most downregulated was adrenomedullin (ADM, FC = -10.12). For 14 altered proteins, no previous direct associations with psoriasis were reported. Among them, DEFB103A_DEFB103B and DSG3 showed the best discrimination between psoriasis and control samples, while SERPINB4 correlated with psoriasis severity. APOA1, DEFB103A_DEFB103B, and DSG3 emerge as novel candidate circulating psoriasis biomarkers, and SERPINB4 as a biomarker of psoriasis severity. The functional role of DSG3 and other newly identified proteins (ACRV1, HAO1, ADH4, GPD1, GFER, PTGES2, DSG3, AFAP1L1, GALNT3, RASGRP2, MAP2K6, LXN, NBEAL2, and VPS54) in psoriasis requires further studies. - Source: PubMed
Publication date: 2026/06/26
Dźwigała MonikaSys DorotaŻycka-Krzesińska JoannaRybicka BeataPopławski PiotrWalecka-Herniczek IrenaPiekiełko-Witkowska AgnieszkaBogusławska Joanna - Glanzmann thrombasthenia (GT) and GT-like phenotype represent inherited platelet disorders caused by defects in platelet glycoprotein αIIbβ3 (encoded by and ) or and -mediated platelet intracellular signaling, respectively. While globally rare, prevalence of these bleeding phenotypes is notably higher in regions with high consanguinity, including Pakistan, with limited data on GT-associated variants. Compared with traditional diagnostic approaches, next-generation sequencing (NGS) offers comprehensive detection of known and novel variants, enhancing diagnostic accuracy in genetically heterogeneous disorders like GT. - Source: PubMed
Publication date: 2026/07/30
Shakoor MadihaAmar AliFarhan SaimaHameed AishaNaveed Muhammad AsifQamar KhansaQadeer Muhammad ImranIbrahim-Kosta ManalAlessi Marie-ChristineKhaliq Shagufta - Deep infiltrating endometriosis (DIE) is a highly fibrotic and deeply invasive subtype of endometriosis that causes severe pelvic pain, infertility and marked impairment of quality of life. Metabolic, microbial and immune disturbances have been reported in women with endometriosis, but whether these systemic perturbations causally contribute to DIE and which lesion-level molecular mediators connect them to pelvic pathology remains unknown. - Source: PubMed
Publication date: 2026/05/21
Shi ShanpingSong WeiWu ZhipingCheng YufengLiu HuaTian FujuLi Xiaocui - Amyotrophic lateral sclerosis (ALS) lacks reliable, disease-specific, and minimally invasive biomarkers, representing a major barrier to early diagnosis and patient stratification. The primary aim of this translational pilot study was to identify a disease-specific, TDP-43-related, gene-microRNA (miRNA) signature in peripheral blood mononuclear cells (PBMCs) of ALS patients with potential diagnostic value. To this end, we first identified differentially expressed disease-specific genes (dsDEGs) using a TDP-43-based rat model of ALS, generated by stereotaxic infusion of full-length (FL) TAR DNA-binding protein 43 (TDP-43) into the motor cortex. Transcriptomic profiling of the motor cortex revealed candidate dsDEGs, which were subsequently validated by RT-qPCR in motor cortex, spinal cord, and PBMCs from the same animals. To assess translational relevance, expression levels of these dsDEGs were analyzed in PBMCs from early- to mid-stage ALS patients and matched healthy controls, while disease specificity was evaluated using Parkinson's disease (PD) samples. In parallel, conserved miRNAs predicted to target the identified dsDEGs were examined in both rat and human PBMCs. Five dsDEGs, Mctp1, Penk, Mt2A, Drd1, and Rasgrp2, were consistently dysregulated across central and peripheral tissues in the TDP-43 rat model. RT-qPCR analysis of human PBMCs confirmed significant and selective dysregulation of these genes in ALS, but not in PD, supporting disease specificity. Moreover, exposure of human neuroblastoma cells and healthy PBMCs to TDP-43 recapitulated the ALS-like expression changes. Computational and experimental analyses identified seven conserved miRNAs targeting these dsDEGs, of which four were significantly downregulated in ALS PBMCs, supporting a coordinated regulatory network. Receiver operating characteristic (ROC) analyses demonstrated strong discriminative performance for both the gene signature (AUC 0.87-1.00) and the associated miRNAs (AUC 0.95-1.00). Together, these findings define a novel PBMC-based gene-miRNA signature that mirrors central ALS pathology and shows high diagnostic accuracy and disease specificity, highlighting its potential as a minimally invasive biomarker for ALS. - Source: PubMed
Publication date: 2026/06/06
Manchinu Maria FrancescaCongiu MichelaMassidda MatteoBorghero GiuseppeMarongiu JacopoMarzi IsabellaMaschio AndreaRallo VincenzoSerra MarcelloPorcedda ClaraEtzi MichelaPalmas Maria FrancescaAngius AndreaSogos ValeriaPateri Maria IdaSteri MaristellaCoroneo ValentinaDe Simone AlfonsoCossu GiovanniChiti FabrizioCarta Anna Rosa - Due to the substantial secretory burden, bovine mammary epithelial cells (BMECs) are highly susceptible to endoplasmic reticulum (ER) stress caused by the accumulation of misfolded proteins when protein-folding capacity is overwhelmed. However, how ATF3 regulates ER stress-induced impairment of milk synthesis and apoptosis in BMECs, particularly through its direct transcriptional targets, remains poorly understood. In this study, we investigated the protective role of activating transcription factor 3 (ATF3) against ER stress-induced impairment of milk synthesis in BMECs. Using a tunicamycin-induced ER stress model, we overexpressed in BMECs and performed integrated RNA-seq and ChIP-seq analyses to elucidate the underlying molecular mechanisms. Our results indicated that ER stress disrupted milk protein and fat synthesis in BMECs by suppressing the expression of CSN2, FASN, FABP3 and promoting apoptosis via upregulation of BAX and CASP3. overexpression effectively attenuated these effects, reducing apoptosis and restoring the expression of milk fat-related genes. Transcriptomics demonstrated that ATF3 activated MAPK and PI3K-Akt signaling and lipid metabolism pathways, significantly upregulating key genes involved in fatty acid uptake, transport, and metabolism (, , , ). Integrated RNA-seq and ChIP-seq analyses identified 81 overlapping genes, with , , , and confirmed as direct transcriptional targets of ATF3, mediating its regulation of the MAPK pathway. Collectively, these findings elucidate the protective role of ATF3 against ER stress-induced lactation disruption and offer potential molecular targets for enhancing lactation resilience in dairy cattle under stress. - Source: PubMed
Publication date: 2026/05/10
Zhang ChenDai WentingLiu YueXu HongweiLiu Hongyun