Polyclonal RANKL
- Known as:
- Polyclonal RANKL
- Catalog number:
- pc-068
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal RANKL
Related genes to: Polyclonal RANKL
- Gene:
- TNFSF11 NIH gene
- Name:
- TNF superfamily member 11
- Previous symbol:
- -
- Synonyms:
- TRANCE, RANKL, OPGL, ODF, CD254
- Chromosome:
- 13q14
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2017-03-02
Related products to: Polyclonal RANKL
Related articles to: Polyclonal RANKL
- Benign airway stenosis (BAS) involves progressive pathological narrowing of the trachea and main bronchi, causing clinically significant respiratory impairment that can advance to life-threatening obstruction. While fibrosis arises from dysregulated immune-stromal crosstalk, the specific cellular and molecular drivers of BAS remain poorly understood. - Source: PubMed
Publication date: 2026/06/16
Liu YifeiJing LeiLuo YukaiChen LuyangJia Qing-ChunChen XiaohuiChen ShaohuaZhang HuapingCheng WenzhaoZhou YunzhiZeng Yiming - Abdominal pain is a hallmark symptom of both inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) and substantially impairs patients' quality of life. Relaxation response-based mind-body intervention (RR-MBI) has been reported to improve disease-specific outcomes and pain catastrophizing in both disorders, accompanied by whole-blood transcriptomic changes. However, the transcriptional features potentially relevant to abdominal pain before and after RR-MBI in IBS and IBD remain insufficiently explored. In this context, this study aimed to analyze these transcriptional changes and prioritize putative abdominal pain-relevant candidate genes from exploratory differentially expressed gene (DEG) sets. - Source: PubMed
Publication date: 2026/06/10
Lin ZhongyuanMo GuohuiWang YiminLin ShiqingGuo Qianqian - Traumatic brain injury (TBI) is a devastating neurological disorder with long-term functional deficits and limited effective therapies, where secondary injury driven by dysregulated immunity and disrupted signaling is pathogenic; Nao Tan Qing (NTQ), a Chinese herbal formula guided by the traditional principle of "resolving phlegm and inducing resuscitation" for "brain collateral obstruction", shows neuroprotective potential, but its role and mechanism in TBI treatment remain unclear. - Source: PubMed
Publication date: 2026/06/14
He RenkeLiu YuhanXiao RuiLin YuqiZhang NiLiu ZhiqiangLi QianqianChen Xuyi - Mesenchymal stem cells (MSCs) and heterogeneous bone marrow stromal cells (BMSCs) are multipotent progenitors that can differentiate into osteoblasts and bone marrow adipocytes (BMAd). The role of BMAd in skeletal homeostasis is not yet fully understood, in part due to a lack of reproducible in vitro models that faithfully mimic the biology and molecular signatures of BMAds to study their behavior. Here, we report the in vitro generation of murine BMSC- and MSC-derived Osterix-expressing BMAd-like cells via a trans-differentiation model (TD-BMAd), the development of a semi-automated analysis platform for quantification of lipid-laden cells, and the use of these models to interrogate the role of the glucocorticoid receptor (GR) in bone marrow adipose tissue (BMAT) as a regulator of osteoclastic bone resorption. The TD-BMAd cells stored intracellular lipids and robustly expressed BMAd-associated genes, such as /Osx, , and . The pro-osteoclastogenic gene /Rankl was comparably expressed between TD-BMAd and osteoblasts. We previously reported that female mice with adult-onset conditional KO (CKO) of the GR in Osx-expressing cells exhibited a low cortical bone mass and high BMAT phenotype. Here, we demonstrate that this phenotype was associated with an increase in the abundance of cortical bone osteoclasts in female but not male GR-CKO mice, but that surprisingly, GR-deficient osteoblasts from these mice did not express higher levels of pro-osteoclastogenic Rankl. Instead, TD-BMAd from female (but not male) GR-CKO mice expressed significantly higher levels of Rankl as compared to cells from GR-WT mice, suggesting that GR-deficient BMAT may be the source of the sexually dimorphic osteoclastogenic phenotype seen in vivo. Although this methodology is not intricate in nature, this simple culture technique and subsequent quantification platform may have broader utility for further studies of BMAd biology and lipid-laden cells. - Source: PubMed
Publication date: 2026/05/17
Lindsay JaeshiaBensreti HusamGross ColbyTripathi AlokMaridas DavidJohnson MaribethShi XingmingBollag Wendy BIsales Carlos MMcGee-Lawrence Meghan E - The global rollout of 5G networks has raised questions regarding the potential biological effects of millimeter-wave exposure, particularly in the skin due to its limited penetration depth. This study examined the effects of whole-body exposure to 27.5 GHz millimeter waves, a frequency within the 5G FR2 bands, on skin-related biological responses in early life mice. Patched1- heterozygous knockout and wild-type CD1 mice were exposed from birth to weaning (P21), 23 h per day, in 10-minute ON/5-minute OFF cycles, at two power densities (6.67 and 20 W/m²). SHAM-exposed animals served as a control. No overt histological abnormalities were observed in exposed skin. However, molecular analyses revealed significant modulation of inflammation-related gene expression. Notably, Ccl4, Csf2, and Tnfsf11 emerged as central regulatory nodes, displaying high degree and betweenness centrality across all groups, irrespective of genotype and sex. Crucially, exposure significantly stimulated mast cell degranulation and, in wild-type mice, led to a reduction in cutaneous glutamate levels. Concurrently, a down-regulation of transcripts associated with cutaneous sensory components (Calca, Mrgprd) was observed within the skin microenvironment. These findings show that 27.5 GHz exposure induces coordinated changes in cutaneous inflammatory pathways and mast cell-mediated homeostasis without detectable structural damage. Overall, these results demonstrate a localized molecular and cellular response within the cutaneous microenvironment, reflecting a subtle homeostatic shift, and suggest that genetic background may contribute to variability in the biological response to millimeter-wave exposure. - Source: PubMed
Publication date: 2026/06/08
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