CD221 Antibody
- Known as:
- CD221 Antibody
- Catalog number:
- XW-7274
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CD221 Antibody
Related genes to: CD221 Antibody
- Gene:
- IGF1R NIH gene
- Name:
- insulin like growth factor 1 receptor
- Previous symbol:
- -
- Synonyms:
- JTK13, CD221, IGFIR, MGC18216, IGFR
- Chromosome:
- 15q26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-07-07
- Date modifiied:
- 2019-04-23
Related products to: CD221 Antibody
Related articles to: CD221 Antibody
- Our study aims to assess the causal association between plasma proteins, immune cell phenotypes and intracerebral hemorrhage (ICH) and explore their downstream biological correlation. - Source: PubMed
Publication date: 2026/04/25
Gu HengBu Yan-SongNiu Jing-JingZhao Hui-MinLi Jia-HeJiang Xiao-TongWu Shu-TongXu Guo-LiYu ShuaiFeng Hong-XuanKong Fan-ZhenWu Guan-Hui - Osteosarcopenia-the concurrent presence of osteoporosis and sarcopenia-affects approximately 18.5% of older adults globally, yet its shared genetic basis remains poorly understood. We applied genomic structural equation modeling (Genomic SEM) to integrate genome-wide association study (GWAS) summary statistics across five phenotypes spanning the pathophysiological spectrum of osteosarcopenia: appendicular lean mass (ALM), bone mineral density (BMD), handgrip strength (HGS), walking pace, and fracture. Fine-mapping, transcriptome-wide association study (TWAS), pathway enrichment, cell-type enrichment, and spatial transcriptomic mapping were performed to functionally annotate the identified loci. A single-factor model (CFI = 0.976) captured the shared genetic liability, with HGS and ALM loading most strongly. A two-factor sensitivity analysis confirmed partial separability of muscle and bone dimensions, though the single common factor was retained for integrated downstream annotation. We identified 58,696 genome-wide significant single-nucleotide polymorphisms (SNPs) condensed into 1078 independent lead variants, including 29 novel loci. Fine-mapping prioritized 317 high-confidence causal variants, encompassing key genes including BMP6, ACAN, IHH, LRP5, and SOX5. TWAS and MAGMA converged on IGF1R, FOXO3, and IRS1 as dual susceptibility genes. Pathway analysis revealed significant enrichment in endochondral ossification and growth hormone/insulin-like growth factor-1 signaling. Cell-type enrichment localized genetic risk to mesenchymal stem cells and skeletal muscle satellite cells, while spatial mapping identified cartilage primordium as the most enriched developmental context. This study systematically elucidates the shared genetic architecture of osteosarcopenia, highlighting developmental, endocrine, and stem cell-related pathways as core mediators. These findings provide a theoretical foundation for precision geroscience and the development of dual-target therapeutic strategies. - Source: PubMed
Publication date: 2026/05/21
Lai WeiqiangGong KaiqinZhong RonghaoYin WeicongLi XuHe XinhuangHu SiyuanChen ChuqunHe KunruiSun ChunhanZheng JianpingZeng Guowei - BMS-754807 is a dual inhibitor of insulin-like growth factor 1 receptor (IGF-1R) and insulin receptor (IR) that is in phase II clinical trials for the treatment of HR-positive and HER2-negative breast cancer. Because IGF-1R signaling regulates inflammatory responses, pharmacological modulation of IGF-1R may have therapeutic potential for Alzheimer's disease (AD); however, the effects of BMS-754807 on neuroinflammatory responses/AD pathology and cognitive function have not been fully investigated. - Source: PubMed
Publication date: 2026/05/20
Lee Hyun-JuSeok JaewooKang SoraOh SeokjunHwang Jeong-WooKim Yu-JinSeo JinsooHoe Hyang-Sook - Premature ovarian insufficiency (POI) is defined by ovarian dysfunction and consequent decreased fertility. While follicular depletion is an acknowledged factor, dynamic changes in follicular subpopulations and single-cell-level niche remodeling remains largely unexplored. Human amniotic epithelial cells (hAECs) represent a promising regenerative approach for restoring ovarian function; however, the underlying mechanism in promoting follicular development remains unclear. - Source: PubMed
Publication date: 2026/05/18
Cao WenjiaoShen LuZhang QinyuHuang YatingSun JunyanCheng ZixinXu JingZhang QiuwanLai Dongmei - Phosphatidylethanolamine binding protein 4 (PEBP4) is a multifunctional protein. The role of intracellular PEBP4 in cancer is well established. However, as a secreted protein, its extracellular functions have yet to be elucidated. Thus, the present study attempted to decipher the functions of the secreted PEBP4. Here, we demonstrated that PEBP4 was upregulated in colorectal cancer (CRC) specimens and was also elevated in the serum of CRC patients. Our results revealed that the secreted PEBP4 (sPEBP4) stimulated the proliferation and migration of colon cancer cells, an event that was prevented by treatment with antibodies against PEBP4 or by mutating the N-glycosylation site (N169 to Q). Our studies indicated that the action of sPEBP4 was different from that of its cellular counterpart. Further, co-injection of the sPEBP4 with colon cancer cells promoted tumorigenesis and lung metastasis in vivo. Mechanistically, sPEBP4 increased phosphorylation of Smad2/3 and Akt/mTOR, which was blocked by the TGFβRⅠ inhibitor SB525334, siRNA or a dominant-negative mutant of TGFβRI, but not by knockdown of IGF-1R or EGFR. In vitro surface plasmon resonance assay revealed that sPEBP4 directly associated with TGFβRs. Finally, sPEBP4 enhanced the stability of TGFβRI by upregulating USP4 through a mechanism similar to TGF-β. Collectively, our study for the first time demonstrates that sPEBP4 activates the TGF-β signaling pathway to promote CRC progression in a TGFβ-independent manner. This would prompt further studies to explore if sPEBP4 could serve as a potential candidate for colorectal cancer therapy or a biomarker for diagnosis, prognosis, and therapeutic responses. - Source: PubMed
Publication date: 2026/05/16
Tang ZhiminLi TingYang ZaiqiZhang YilanZhou YanDeng XiaohuiChen WenyuHuang DeqiangZhu LingyanYan XiaohuaShao HengyiLuo ZhijunLuo Lingyu