Human IGF-1R _CD221 Protein Vector: HEK293
- Known as:
- Human IGF-1R _CD221 Protein Vector: HEK293
- Catalog number:
- 10138-H01H
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human IGF-1R _CD221 Protein Vector: HEK293
Related genes to: Human IGF-1R _CD221 Protein Vector: HEK293
- 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
- Gene:
- IRAIN NIH gene
- Name:
- IGF1R antisense imprinted non-protein coding RNA
- Previous symbol:
- -
- Synonyms:
- IGF1R-AS
- Chromosome:
- 15q26.3
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2014-08-07
- Date modifiied:
- 2019-04-23
Related products to: Human IGF-1R _CD221 Protein Vector: HEK293
Related articles to: Human IGF-1R _CD221 Protein Vector: HEK293
- To identify baseline gene expression programs associated with recurrence timing in estrogen receptorpositive (ER+) breast cancer (BC) using a multi-state modeling framework. - Source: PubMed
Publication date: 2026/06/30
Wang YongzheQuinones ChristineKang IreneRugo HopeMartinez ErnestSeewaldt VictoriaMortimer JoanneNath AritroJones Veronica - Breast cancer is the most common cancer in women and the second most frequent cancer worldwide. Changes in miRNA levels are associated with various diseases, including cancer, making them ideal non-invasive biomarkers for diagnosis, prognosis, and treatment. Bioinformatics advancements have enabled the prediction of miRNAs and their target genes. This study aimed to analyze the miR-15 family (miR-15a, miR-15b, miR-16-1, miR-16-2, miR-195, and miR-497) to predict their target genes and evaluate their role in breast cancer progression. - Source: PubMed
Publication date: 2026/05/29
Alizadeh MahdiSalimi Mahdieh - Small cell lung cancer (SCLC) exhibits extreme numbers of circulating tumor cells (CTCs) that are operative in tumor dissemination and possibly drug resistance, ultimately resulting in a dismal prognosis. Tumor cells depend on kinases, which are triggered by a range of growth factors for their malignant proliferation. Insulin-like growth factor-I receptor (IGF-1) and vascular endothelial growth factor receptor (VEGFR), c-Kit, epidermal growth factor receptor (EGFR), as well as downstream signaling transmitters such as phosphoinositide 3-kinase (PI3K), Akt and the mammalian target of rapamycin (mTOR) and a range of other kinases were investigated as potential anti-tumor targets in SCLC. Despite the expression of rational targets, the studies with tyrosine kinase inhibitors (TKIs) in SCLC have been very disappointing in the clinic. The preclinical activity of kinase inhibitors against native and resistant SCLC cell lines failed to predict efficacy in patients. Screening of a kinase inhibitor library showed activity of most compounds against single SCLC CTC cells but high chemoresistance of BHGc10 spheroids (termed tumorospheres). Only a few hydrophobic multitarget inhibitors proved active against the spheroids, and drugs that failed in clinical trials targeting IGF-1R, AURORA kinase and Polo kinases showed low activity against CTC tumorospheres. These results demonstrate that for SCLC, kinase inhibitors should be tested against spheroids to obtain a better prediction of their potential clinical activity. - Source: PubMed
Gerhard HamiltonEggerstorfer Marie-ThereseStickler Sandra - Cryptorchidism, a major reproductive malformation in dogs, is associated with an increased risk of testicular cancer. In this study, we aimed to compare miRNA expression and 3'UTR length variation in the mRNAs of differentially expressed genes (DEGs) between undescended (UD) and descended (D) canine testes without signs of tumorigenesis. In total, expression of 453 miRNA genes was detected, and over 100 miRNA DEGs were identified in the UD vs. D and UD vs. C (control) comparisons. Predicted target sequences for DEG miRNAs were in silico identified in numerous mRNAs, including 12 of 19 a priori selected genes related to testicular cancer. In silico analysis of miRNA and mRNA DEGs revealed that some of target mRNAs showed significant differences in UD and D/C testes and approximately 50% of miRNA-mRNA pairs exhibited an inverse expression pattern, including cancer-related genes (e.g., AR, IGF1R, KIT, KITLG, SALL4, and SPRY4). Analysis of the 3'UTR length of DEG mRNAs identified 962 transcripts with altered 3'UTR length in both the UD vs. D and UD vs. C comparisons. 3'UTR lengthening (e.g., in cancer-related genes such as LATS2, SRPK2, and AKT3) was the most common alteration observed. Our findings provide a new insight into molecular alterations associated with canine cryptorchidism. We suggest that in undescended canine testes without signs of tumorigenesis dysregulated expression of protein-coding genes, including candidate cancer-associated genes, can be associated with altered expression of specific miRNAs, as well as variations in the 3'UTR length of certain target DEG mRNAs. - Source: PubMed
Publication date: 2026/07/06
Nowacka-Woszuk JoannaKajdasz ArkadiuszStachowiak MonikaSzczerbal IzabelaSwitonski Marek - Owing to drug resistance to therapeutic targets, there is an urgent demand to find and validate new potent targets for non-small cell lung cancer (NSCLC). Although high SALL4 expression significantly promotes lung cancer growth, its oncogenic mechanism remains unclear. In the current study, focal adhesion molecular focadhesin (FOCAD), a candidate that has interacted with oncofetal SALL4, was identified by SALL4 immunoprecipitation and mass spectrometry. Immunoprecipitation, immunofluorescence stains, cell component separation, and molecular docking demonstrated the interaction of SALL4 and FOCAD. Immunoblotting and/or TCGA dataset analysis showed high expression of SALL4 and FOCAD paralleled in lung adenocarcinoma but not in lung squamous cell carcinoma. FOCAD knockdown resulted in dramatic inhibition of cell viability, colony formation, xenograft growth, wound healing, and invasion; apoptotic induction; and G-phase blockade in NSCLC cell lines through suppression of the EGFR or IGF1R signaling pathways and expression of FAK and β-catenin. Conversely, SALL4 overexpression partially attenuated the inhibition of cell viability and colony formation of FOCAD silencing in these cells. The combination of FOCAD shRNA knockdown with osimertinib treatment showed additive anti-tumor activity in NSCLC cell lines. Furthermore, FOCAD silencing also showed markedly anti-proliferative effects in the osimertinib-resistant NSCLC cell line. These findings demonstrate that FOCAD in NSCLC is generally associated with SALL4 and EGFR expressions and activation. There are functional correlations between FOCAD and SALL4, and targeting FOCAD could be an effective therapeutic strategy in both osimertinib-sensitive and -resistant NSCLC. - Source: PubMed
Publication date: 2026/07/04
Lu XinGu YijieYe WeiWang HaitaoOu Wen-Bin