Polyclonal Rabbit CST2 Antibody
- Known as:
- Polyclonal Rabbit CST2 Antibody
- Catalog number:
- KA0924
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit CST2 Antibody
Related genes to: Polyclonal Rabbit CST2 Antibody
- Gene:
- CST2 NIH gene
- Name:
- cystatin SA
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1990-02-06
- Date modifiied:
- 2016-10-05
Related products to: Polyclonal Rabbit CST2 Antibody
Related articles to: Polyclonal Rabbit CST2 Antibody
- This study addresses the dual issues of natural sand depletion and the surge in construction and demolition waste by improving recycled fine aggregate (RFA) through optimised CO curing for use in both Portland pozzolanic cement (PPC) and one-part geopolymer mortars. Using the Taguchi L9 design, carbonation parameters-time, temperature, relative humidity, and CO concentration were statistically optimised to enhance process efficiency. The optimal condition of 24 h at 30 °C, 65% RH, and 15% CO markedly improved specific gravity and bulk density while lowering water absorption, confirming effective pore refinement in RFA. Silica gel and lime-assisted treatments further enhanced carbonation efficiency. The 3% silica gel-pre-soaked aggregate (CST2) achieved superior CO uptake and surface densification, while lime pre-treatment also produced notable improvements. The reported CO uptake values were quantitatively derived from thermogravimetric analysis by converting the mass loss associated with CaCO decomposition into equivalent CO content, enabling direct evaluation of carbonation efficiency. In PPC mortars, optimised RFA restored the strength loss typical of untreated aggregates, while in geopolymer mortars, CST2 and lime-treated RFA yielded up to 44% higher compressive strength, reflecting better binder-aggregate compatibility. Microstructural analyses (TGA, XRD, FTIR, SEM/EDS) confirmed the formation of a CaCO layer and an improved ITZ structure, while leachate tests indicated reduced pH and lower chromium release. Overall, the study offers a sustainable pathway for CO utilization and high-performance RFA production for durable, low-carbon cementitious systems. - Source: PubMed
Publication date: 2026/04/27
Poojalakshmi E SShaju Anila CNagarajan PraveenSudhakumar JThomas Blessen SkariahDas SudhaBerhe Missgna Addisalem - Esophageal cancer (ESCA) is a common gastrointestinal tumor with high incidence and metastatic potential. Cystatin 2 (CST2) has been identified as a carcinogenic factor that regulates the progression of esophageal squamous cell carcinoma (ESCC). However, its role in ESCA progression and the underlying molecular mechanisms require further investigation. - Source: PubMed
Publication date: 2026/04/23
Chen FangYu LonghaiWang DechangZhao YongLi Chuanchen - Smoking is a preventable cause of colorectal cancer (CRC), and nicotine metabolism may promote tumorigenesis. We aimed to investigate the prognostic significance of nicotine metabolism‑related genes (NRGs) in colon adenocarcinoma (COAD) and to develop a gene signature for patient stratification. - Source: PubMed
Publication date: 2026/02/11
Li JunliangZhang JunyiWang DanningShen JieyiShen ChongZeng WeiqiWang Jianwei - Hippo is the namesake component of a conserved transduction cascade/regulator of tissue homeostasis and development across metazoans. The Ste20-family kinase Hippo/MST activates the NDR-family kinase Warts/LATS to inhibit the transcriptional coactivator Yorkie/YAP/TAZ and its transcription factor partner Scalloped/TEAD. In Caenorhabditis elegans, cell lineages and organ sizes are largely invariant, and classical Hippo phenotypes such as tissue overgrowth are absent. Nevertheless, WTS-1, YAP-1, and the TEAD-like transcription factor EGL-44 form a conserved core module required for larval development past the L2 stage. Crucially, a direct role for Hippo signaling remains unestablished. To address this question, we generated a fluorescently tagged endogenous YAP-1 as a live biomarker of pathway activity. Upon WTS-1 loss, endogenous YAP-1 translocated from cytosol to nucleus in the epithelium and intestine. Tissue-specific depletion revealed that intestinal but not epithelial WTS-1 is essential for progression past L2. The duplicated Hippo-related kinases CST-1 and CST-2 repressed YAP-1 nuclear localization in the epithelium but not the intestine, indicating that intestinal WTS-1 functions without CST-1/2. The Ste20 kinase MIG-15, orthologous to Drosophila Misshapen and mammalian MAP4K4/6/7, was redundant with CST-1/2 for larval progression. Yet deficient MIG-15 uniquely increased YAP-1 abundance without driving nuclear localization. In contrast, the Ste20 kinase GCK-2, orthologous to Drosophila Happyhour and mammalian MAP4K1/2/3/5, had no detectable role. Our findings establish C. elegans as a model for Hippo signaling, with Hippo-dependent and Hippo-independent cascades controlling WTS-1 in epithelia and intestine, respectively. In this context, YAP-1/EGL-44 outputs are repurposed from the conventional association with growth control to nonproliferative developmental functions. - Source: PubMed
Huynh LinhFakieh Razan AHendrix C'BrionnePowell Reid TReiner David J - Lung cancer patients with interstitial pneumonia (IP) have limited treatment options due to the risks associated with therapeutic intervention. The underlying causes of IP in these patients are diverse, and there is currently no detailed molecular pathological classification or an established understanding of the effectiveness of anti-fibrotic medications such as nintedanib. This study aimed to elucidate the mechanism of action of nintedanib by analyzing differential RNA expression between normal and fibrotic lung tissues from lung cancer patients with IP. - Source: PubMed
Publication date: 2026/02/05
Kuroda HiroakiMasago KatsuhiroSeto KatsutoshiHorio YoshitsuguSasaki EiichiFujita ShiroMatsushita Hirokazu