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
- To explore the roles of insulin-like growth factor 1 receptor (IGF1R) and thyroid-stimulating hormone receptor (TSHR) in extraocular muscle pathology. - Source: PubMed
Publication date: 2026/09/18
Chen Kuan-YingLin Chia-ChenChen Wan-JuLai Chun-Chieh - Drug repurposing can accelerate the identification of novel therapeutic candidates for rare cancers such as inflammatory breast cancer (IBC), an aggressive type with limited therapeutic options. Here, we report an experimental validation study of compounds previously identified through two computational approaches: Literature Wide Association Studies (LWAS) and Gene Reversal Rate (GRR). Candidate compounds were tested using orthogonal cell viability assays in 2D models across IBC and non-IBC cell lines. In the SUM149 IBC cell line, repurposed compounds predicted from LWAS achieved a 70% success rate, with several showing nanomolar potency, while those predicted from GRR showed a 38% success rate. Through systematic combination screening in both 2D and 3D-spheroid SUM149 models, we identified novel synergistic compound pairs targeting crosstalk between IGF-1R, EGFR and PI3K/Akt/mTOR pathways, with high synergy scores across multiple reference models. Using these combinations, western blott analysis revealed significant suppression in the phosphorylation of key signaling proteins and downstream effectors, while wound healing assays showed reduced cell migration with some combination treatments, suggesting effective pathway inhibition. To further validate these findings at the transcriptional level, RNA-Seq analysis in SUM149 cells confirmed that the GRR drug combinations significantly reversed the IBC gene expression signature (IBC-GES) and identified several clinically relevant genes whose expression was significantly altered. Together, these findings validate our computational predictions and identify candidate combination strategies that may help address therapeutic resistance in IBC. This integrated computational-experimental approach establishes a pipeline for systematic drug repurposing and highlights novel therapeutic combinations for further investigation. - Source: PubMed
Publication date: 2026/09/16
Salim Esraa AJi XiaojiaTarpley MichaelDixon Maria SZheng WeifanScott John EWilliams Kevin P - -associated skeletal dysplasias affect cartilage extracellular matrix and endochondral growth, but patient growth-plate tissue is largely inaccessible. We generated chondrogenically induced urine-derived cells (chUDCs) from three individuals with heterozygous pathogenic variants and three healthy controls. Classical differentiation was assessed by Alcian blue and Alizarin red staining, bulk RNA sequencing compared patient-derived and control chUDCs, and single-cell RNA sequencing was performed in two patient-derived lines. -mutant chUDCs retained overt chondrogenic and osteogenic staining capacity without a clear patient-control separation. In contrast, bulk RNA sequencing identified a small set of consistently differential extracellular-matrix remodeling genes enriched for matrix and ossification-related programs; and remained significant in leave-one-donor-out, age-adjusted and cell-composition-adjusted models. Single-cell profiling resolved multiple chUDC states, including chondrogenic, fibroblastic extracellular-matrix, IGF1R-high, and osteogenic-associated states. IGF1 co-treatment was associated with reduced osteogenic-associated module scores and increased fibroblastic/anabolic extracellular-matrix programs. Because no IGF1-treated control-donor line was profiled, IGF1-associated changes are reported as exploratory and are not claimed to be -specific. These findings support chUDCs as a non-invasive system for exploring selected transcriptional programs relevant to cartilage biology and growth-factor responsiveness in -associated growth disorders. - Source: PubMed
Publication date: 2026/09/01
Schulz AlexanderSchubert MichaelBrockmann Emily MEkici Arif BUebe SteffenThiel Christian T - Salivary gland neoplasms (SGNs) represent a diverse group of benign and malignant tumors characterized by distinct genetic abnormalities that contribute to their pathogenesis and variable clinical behavior. This review synthesizes current evidence on the molecular alterations underlying SGNs and highlights emerging therapeutic targets with translational potential. A comprehensive literature search was conducted across PubMed, Google Scholar, Cochrane, and SCOPUS for studies published between 1990 and 2025, focusing on genetic aberrations, oncogenic fusions, and targeted treatment strategies. Data reveal that small molecule inhibitors and other targeted agents may offer promising alternatives to conventional chemotherapy. For instance, pleomorphic adenomas often have PLAG1 overexpression and FGFR1 fusions, activating the IGF and WNT signaling pathways; linsitinib, a dual IGF1R and tyrosine kinase inhibitor, has demonstrated antitumor activity in other malignancies and may hold potential in this context. Similarly, alterations in EGFR, HER2, and PI3K pathways across multiple salivary tumor subtypes highlight opportunities for small molecular inhibitor therapy. However, current data remain limited, and therapeutic applications are largely extrapolated from other cancers. Further research is needed to validate these findings in clinical trials. Overall, integrating molecular diagnostics with pathway-specific targeted therapies may enhance outcomes and expand treatment options for patients with SGNs. - Source: PubMed
Publication date: 2026/09/15
Kota SharwaniSmith Richard V - Thyroid eye disease (TED) is a complex autoimmune disorder and the most common extrathyroidal manifestation of Graves' disease, characterized by orbital inflammation, tissue remodelling, and varying degrees of functional and cosmetic impairment. Although often mild, moderate-to-severe and sight-threatening forms can significantly compromise vision and quality of life. Advances in the understanding of TED pathophysiology - particularly the roles of orbital fibroblasts, thyrotropin receptor and insulin-like growth factor 1 receptor signalling- have transformed its diagnostic and therapeutic landscape. This manuscript provides a comprehensive and updated overview of epidemiology, risk factors, clinical presentation, diagnostic evaluation and management of TED. Current treatment strategies emphasize early risk-factor modification, restoration of euthyroidism, and a multidisciplinary approach tailored to disease activity and severity. Intravenous glucocorticoids remain the cornerstone of therapy for active moderate-to-severe disease, whereas adjunctive immunosuppressive agents and orbital radiotherapy are used in selected cases. The advent of targeted biologic therapies, particularly teprotumumab, as well as rituximab and tocilizumab, has significantly expanded therapeutic options and enabled a more personalized, phenotype-driven approach. Surgical rehabilitation continues to play a pivotal role in the inactive phase. Emerging therapies targeting novel molecular pathways hold promise for further improving patient outcomes. Despite these advances, challenges related to accessibility, cost, long-term safety and optimal patient selection persist. Ongoing research and international collaboration are expected to refine management strategies and enhance the quality of life of patients with TED. - Source: PubMed
Publication date: 2026/08/31
Markantes Georgios KEffraimidis GrigorisKarapanou OlgaSaltiki KaterinaMichalaki Marina