Calb2 Antibody (OASA09088)
- Known as:
- Calb2 Antibody (OASA09088)
- Catalog number:
- oasa09088
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Calb2 Antibody (OASA09088)
Related genes to: Calb2 Antibody (OASA09088)
- Gene:
- CALB2 NIH gene
- Name:
- calbindin 2
- Previous symbol:
- -
- Synonyms:
- CAL2
- Chromosome:
- 16q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2015-08-24
Related products to: Calb2 Antibody (OASA09088)
Related articles to: Calb2 Antibody (OASA09088)
- It remains unclear how circulating tumor cells (CTCs) adapt to and survive mechanical forces in the bloodstream, including fluid shear stress (FSS), making it critical to define the mechanisms that enable their survival and promote metastasis. To model these forces, we generated "mechanoresistant" (MR) LNCaP and PC3 prostate cancer (PCa) cell lines by repeatedly exposing cells to high‑intensity (HI) FSS (3950 dyn/cm). LNCaP MR cells acquired marked resistance to HI FSS, exhibiting significantly reduced apoptosis, while PC3 cells demonstrated innate resistance. Bulk RNA‑sequencing revealed that LNCaP and PC3 MR cells developed distinct molecular programs. CALB2 (calretinin) emerged as a mechanoresistance gene selectively upregulated in PC3 MR cells, and CALB2 knockout significantly reduced viability upon re‑exposure to HI FSS. Analysis of CALB2‑high PCa cases captured patient‑level molecular heterogeneity, suggesting a mechanoadaptive state rather than a uniform aggressiveness-driven tumor phenotype. This was consistent with the absence of correlation between CALB2 levels and Gleason Scores. In an orthotopic PCa mouse model, the PC3 MR condition displayed the most aggressive early tumor growth and the largest endpoint tumor volumes, consistent with enhanced proliferation. Together, these findings demonstrate that PCa cells acquire discrete mechanoadaptive phenotypes under extreme FSS, revealing targetable pathways to limit metastatic competence. - Source: PubMed
Publication date: 2026/07/20
Fabiano Abigail RLuo Allen CTaufalele PaulDombroski Jenna AAalaei EhsanRowland Schyler JCantú Melissa SCarter Alexandria TKnoblauch Samantha VReinhart-King Cynthia AKing Michael R - Variants in the CNTNAP2 gene, encoding the cell adhesion molecule CASPR2, have been identified as genetic risk factors for autism spectrum disorder (ASD). However, the mechanisms through which CNTNAP2 dysfunction alters circuit function remain unknown. Interneurons, as key regulators of excitatory-inhibitory balance, represent a candidate source of vulnerability. In this study, we quantified calretinin-positive (CR+) and parvalbumin-positive (PV+) interneuron density in the caudoputamen (CP) and somatosensory cortex (SSC) of Cntnap2 knockout (KO) and wild-type (WT) mice and assessed their relationship with social behavior. Cntnap2 KO mice exhibited significantly lower CR+ interneuron density in both brain regions, whereas no significant difference was observed in the PV+ density. Cntnap2 KO females showed altered behavior in the social novelty preference test compared to WT females. Cntnap2 KO animals also displayed elevated "moving away" responses, a social withdrawal phenotype. Correlation analyses revealed that within the KO group, higher striatal CR+ density was associated with a greater frequency and duration of "moving away." CR+ density in the SSC did not correlate with this behavioral phenotype. The results suggest that striatal CR+ interneurons may modulate the persistence and intensity of social withdrawal behavior. In conclusion, our findings reveal region-specific alterations in CR+ interneuron density in Cntnap2 KO mice and uncover a previously unrecognized link between Cntnap2 function, striatal interneuron organization and social withdrawal behavior. The results highlight CR+ interneurons as potential contributors to altered basal ganglia function in ASD and underscore the need for circuit-level analyses of genetically defined risk models. - Source: PubMed
Publication date: 2026/06/06
Sáfár KrisztinaSzendi VivienHoppa PaulinaWang YutongSeres Fanni ÁBartók SzilviaTeadora TylerShi LeiDobolyi ÁrpádPuska GinaAdorján István - : Globally, colorectal adenocarcinoma (COAD) continues to be one of the most frequent contributors to cancer-associated deaths, pointing out an ongoing demand for robust biomarkers capable of reflecting disease advancement and predicting patient outcomes. Calbindin 2 (CALB2), a calcium-binding protein, has been implicated in tumor progression in several malignancies, but the precise functional involvement of this molecule in COAD remains insufficiently characterized. This study aimed to examine the clinical relevance and functional significance of CALB2 in COAD. : Clinical tissue-based analyses, bioinformatic analyses of publicly available datasets, in vitro and in vivo functional assays, and targeted metabolomic profiling were performed to evaluate CALB2 in COAD. : Immunofluorescence analysis of a COAD tissue microarray revealed that CALB2 expression was more frequently detected in stage III tumors and was associated with the proliferation marker Ki67. The Cancer Genome Atlas (TCGA) cohort's bioinformatic analyses revealed an increase in CALB2 expression with advancing pathological T stage, and it was associated with poorer overall survival. Functional experiments demonstrated that CALB2 expression accelerated tumor growth in vivo and promoted the migration and proliferation of colorectal adenocarcinoma cells in vitro. At the molecular level, altered CALB2 expression was associated with changes in epithelial-mesenchymal transition-related markers, p53 Ser33 phosphorylation, and amino acid-related metabolic profiles. : Collectively, these findings show a correlation between CALB2 expression and poor clinical outcomes and disease progression in colorectal adenocarcinoma. - Source: PubMed
Publication date: 2026/04/25
Yang FengLiu YizhouLuo NaLi QianxiaHu Guangyuan - Microsampling using filter cards for dried blood spots (DBS) and dried plasma spots (DPS) is a well-established technique offering practical advantages for blood collection and subsequent processing. For DBS/DPS, only a small sample volume is required it enables transport and storage at ambient temperature, and it is well suited for decentralized sample collections and resource-limited settings, as well as collection from elderly individuals, when venous blood collection might be problematic. Many protein-based biomarker assays like enzyme-linked immunosorbent assays (ELISA) depend on blood, plasma, or serum as sample matrix. Calretinin is an established biomarker for the early detection of mesothelioma. Herein, we investigated whether DPS are suitable for the determination of calretinin protein by ELISA in comparison to commonly used plasma samples. - Source: PubMed
Publication date: 2026/05/25
Gleichenhagen JanKaiser NinaBrüning ThomasJohnen GeorgWeber Daniel G - Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by core symptoms including impairments in social behavior and communication. The impaired excitatory and inhibitory signals have been implicated in the pathophysiology of social behavior deficits. Altered calretinin (CR)-containing GABAergic interneurons have been observed in ASD, but their roles and underlying mechanisms remain unveiled. Here, using valproic acid (VPA)-exposed mice for CR-Cre and R26::LS-tdTomato (Ai14) model of ASD, we prove that a decreased number of CR interneurons in the mPFC of an animal model for ASD. Double-staining experiments demonstrated the decreased number of CR interneurons stained for c-Fos. Also, reduction in GCaMP7s fluorescence intensity was elicited in sociability and social novelty preference using in vivo fiber photometry, manifesting VPA-induced suppression of CR-positive cell activation. Additionally, we observed the abnormalities of dendrites in CR interneurons including lower dendritic arbors, decreased dendrite complexity, and spine density, paralleled by abnormal development of spine morphology. Intriguingly, the electrophysiological recordings of tdTomato-labeled interneurons revealed that exposure to VPA depressed intrinsic neuronal excitability by decreasing spontaneous and evoked action potential frequencies. These changes were concomitant with impairments of glutamatergic and GABAergic synaptic transmission of CR interneurons. Strikingly, chemogenetic silencing of mPFC CR-expressing interneurons induced social interaction deficits in mice. These sociability impairments can be rescued by optogenetic activation of CR activity in VPA-exposed mice. Our study indicates that prenatal exposure to VPA induced reduced activities, abnormalities in morphological development, and decreased intrinsic excitability as well as accompanying impaired synaptic transmission of CR interneurons. Our findings provide strong evidence for the notion that the CR interneurons has a critical role in the regulation of social behavior in mice and manifest that CR interneurons dysfunction may be implicated in social impairments in ASD. - Source: PubMed
Publication date: 2026/05/21
Chen MengyuanZhao KeGao ChaoMei DaoqiShi ShengliWang LiSun LiminGuo JishengBin GuoZhao ShuaiYan XingxueHe MiaoZhang YaodongWang Xiaona