KLLN antibody
- Known as:
- KLLN (anti-)
- Catalog number:
- orb100624
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- KLLN antibody
Related genes to: KLLN antibody
- Gene:
- KLLN NIH gene
- Name:
- killin, p53 regulated DNA replication inhibitor
- Previous symbol:
- -
- Synonyms:
- killin
- Chromosome:
- 10q23
- Locus Type:
- gene with protein product
- Date approved:
- 2011-02-18
- Date modifiied:
- 2019-04-23
Related products to: KLLN antibody
Related articles to: KLLN antibody
- Pituitary adenoma (PA) is a chronic endocrine disease leading to various physiological abnormities. Our previous study has revealed that PA would result in thyroid diseases including goiter and thyroid cancer, which are caused by increased proliferation and tumorigenic potential of thyroid cells. However, the mechanism of PA inducing thyroid diseases remains unclear. Our recent study has indicated that insulin-like growth factor I (IGF-I) might be positively correlated with thyroid diseases in PA patients. Therefore, the primary aim of this study was to investigate the mechanism of PA-induced IGF-I triggering increased proliferation and tumorigenic potential of thyroid cells. In this study, cell proliferation was detected using CCK-8 assay, clone formation ability was identified by clone formation assay, and nude mice xenograft tumor model was established to determine the tumorigenicity of IGF-I-treated thyroid cells in vivo. The current study confirms that IGF-I is positively associated with thyroid diseases in PA patients. Besides, IGF-I is found to promote thyroid cell proliferation and increase tumorigenic potential of thyroid cells by decreasing Killin (KLLN). Moreover, IGF-I declines KLLN by activating MET proto-oncogene, receptor tyrosine kinase (MET) in thyroid cells. Additionally, IGF-I-activated MET reduces KLLN by suppressing KLLN transcription via repressing tumor protein 53 (TP53) in thyroid cells. These findings uncover that the PA-dependent IGF-I/MET/TP53/KLLN signaling axis contributes to increased proliferation and tumorigenic potential of thyroid cells, which should provide potential therapeutic targets for thyroid diseases in PA. - Source: PubMed
Publication date: 2026/04/04
Guo XiaoyuYang LeiZhong JianxiangWu BolinYang ChengyouWu JiamingWang XiaoXie YanhongZhang RongZhang JianpingDu QiuChen Zhiyong - [This corrects the article DOI: 10.1155/2021/9970272.]. - Source: PubMed
Publication date: 2025/09/04
- Breast cancer (BC) is the most common cancer and the leading cause of cancer death in women. Hereditary BC risk accounts for 25% of all cases. Pathological variants in known BC precursor genes explain only about 30% of hereditary BC cases, while the underlying genetic factors in most families remain unknown. Identifying hereditary cancer risk factors will help improve genetic counseling, cancer prevention, and cancer care. Here, we used whole-exome sequencing (WES) to identify genetic variants in 105 Vietnamese patients with BC and 50 healthy women. BC-associated variants were screened by the Franklin software and the criteria of the American College of Medical Genetics and Genomics (ACMG) and evaluated based on in silico analysis. In total, 56 variants were identified in 37 genes associated with BC, including , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , and in 41 patients. Among them, 12 variants were novel, and 10 variants were assessed as pathogenic/likely pathogenic by ACMG and ClinVar. Variants of uncertain significance (VUS) were evaluated using in silico prediction software to predict whether they are likely to cause the disease in patients. This is the first WES study to identify BC-associated genetic variants in Vietnamese patients, providing a comprehensive database of BC susceptibility gene variants. We suggest using WES as a tool to identify genetic variants in BC patients for risk prediction and treatment guidance. - Source: PubMed
Publication date: 2025/08/28
Van Tung NguyenLien Nguyen Thi KimHuan Le DucPhuong Pham CamMai Bui BichMai Nguyen Thi HoaHuong Tran Thi ThanhHuyen Phung ThiVan Chu NguyenVan Dung TranHuy Luu HongKien Dong ChiManh Dang VanLong Duong MinhLan Nguyen NgocHien Nguyen ThanhHanh Ha HongHoang Nguyen Huy - Somatic variants causing epilepsy are challenging to detect, as they are only present in a subset of brain cells (e.g., mosaic), resulting in low variant allele frequencies. Traditional methods relying on surgically resected brain tissue are limited to patients undergoing brain surgery. We developed an improved protocol to detect somatic variants using DNA from stereoelectroencephalographic (SEEG) depth electrodes, enabling access to a larger patient cohort and diverse brain regions. This protocol mitigates issues of contamination and low yields by purifying neuronal nuclei using fluorescence-activated nuclei sorting (FANS). - Source: PubMed
Publication date: 2025/01/03
Mascarenhas RumikaMerrikh DariaKhanbabaei MaryamKaur NavprabhjotGhaderi NavidMaroilley TatianaLiu YipingSoule TylerAppendino Juan PabloJacobs JuliaWiebe Samuel Hader WalterPfeffer GeraldTarailo-Graovac MajaKlein Karl Martin - LncRNAs regulate tumorigenesis and development in a variety of cancers. We substantiate for the first time that LINC00606 is considerably expressed in glioblastoma (GBM) patient specimens and is linked with adverse prognosis. This suggests that LINC00606 may have the potential to regulate glioma genesis and progression, and that the biological functions and molecular mechanisms of LINC00606 in GBM remain largely unknown. - Source: PubMed
Publication date: 2024/05/09
Dong NaijunQi WenxinWu LinglingLi JieZhang XueqiWu HaoZhang WenJiang JiawenZhang ShiboFu WenjunLiu QianQi GuandongWang LukaiLu YanyuanLuo JingyiKong YanyanLiu YihaoZhao Robert ChunhuaWang Jiao