Ask about this productRelated genes to: Slc9a3r2 Blocking Peptide
- Gene:
- SLC9A3R2 NIH gene
- Name:
- SLC9A3 regulator 2
- Previous symbol:
- -
- Synonyms:
- SIP-1, TKA-1, NHERF-2, E3KARP
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-26
- Date modifiied:
- 2016-02-18
Related products to: Slc9a3r2 Blocking Peptide
Related articles to: Slc9a3r2 Blocking Peptide
- The molecular mechanisms driving the occurrence and progression of breast cancer remain unclear, necessitating the identification of novel molecular biomarkers and therapeutic targets. This study aims to investigate the role of () in breast cancer progression via an integrated multi-scale approach. Analysis of The Cancer Genome Atlas (TCGA) data revealed that is upregulated at both protein and mRNA level in breast cancer tissues, related to advanced tumor stage and poor prognosis, especially in luminal subtypes. Functional enrichment analyses linked high expression to epithelial-mesenchymal transition (EMT), estrogen response, and PI3K-AKT/MAPK signaling pathways. Additionally, expression was negatively correlated with the infiltration level of CD8+ T cell as well as the expression of four main immune checkpoint molecules. Single-cell RNA sequencing analysis of patient samples revealed that -positive tumor epithelial cells mediate aberrant cellular communication with endothelial cells, fibroblasts, and macrophages via specific ligand-receptor pairs involving , and . Cell functional assays showed that knockdown of significantly impaired the proliferation, migration, and invasion capacities of breast cancer cells. Our findings establish as a key promoter of breast cancer progression, influencing both intrinsic oncogenic pathways and the extrinsic tumor microenvironment (TME), which provides a novel insight for breast cancer treatment. - Source: PubMed
Publication date: 2026/05/11
Chen ZujinWang YaoWang GuixinYu YueWang XinCao Xuchen - The present study aimed to clarify the clinical significance of the cell-free DNA (cfDNA) methylation profile of patients with non-small cell lung cancer (NSCLC) showing the epidermal growth factor receptor (EGFR) gene mutation. - Source: PubMed
Publication date: 2025/04/25
Fujimoto MaoYasuda HiroyukiArai EriNakajima MakotoTakata SaoriMorikawa KeiTanaka HisashiItani HidetoshiHonda TakeshiHoriuchi KazuyaWatanabe KageakiNakagawa HideyukiNakahara YoshiroSeki YoshitakaBessho AkihiroTakahashi NobumasaHayashi KentaroEndo TakeoTakeyama KiyoshiMaekura ToshiyaTakigawa NagioKawase AkikazuEndoh MakotoNemoto KenjiKishi KazumaSoejima KenzoOkuma YusukeTogashi AkiraMatsutani NoriyukiSeki NobuhikoKanai Yae - Kohlschütter-Tönz syndrome (KTS) is a rare autosomal recessive disorder characterized by severe intellectual disability, early-onset epileptic seizures, and amelogenesis imperfecta. Here, we present a novel Rogdi mutant mouse deleting exons 6-11- a mutation found in KTS patients disabling ROGDI function. This Rogdi mutant model recapitulates most KTS symptoms. Mutants displayed pentylenetetrazol-induced seizures, confirming epilepsy susceptibility. Spontaneous locomotion and circadian activity tests demonstrate Rogdi mutant hyperactivity mirroring patient spasticity. Object recognition impairment indicates memory deficits. Rogdi mutant enamel was markedly less mature. Scanning electron microscopy confirmed its hypomineralized/hypomature crystallization, as well as its low mineral content. Transcriptomic RNA sequencing of postnatal day 5 lower incisors showed downregulated enamel matrix proteins Enam, Amelx, and Ambn. Enamel crystallization appears highly pH-dependent, cycling between an acidic and neutral pH during enamel maturation. Rogdi teeth exhibit no signs of cyclic dental acidification. Additionally, expression changes in Wdr72, Slc9a3r2, and Atp6v0c were identified as potential contributors to these tooth acidification abnormalities. These proteins interact through the acidifying V-ATPase complex. Here, we present the Rogdi mutant as a novel model to partially decipher KTS pathophysiology. Rogdi mutant defects in acidification might explain the unusual combination of enamel and rare neurological disease symptoms. - Source: PubMed
Publication date: 2024/01/03
Jimenez-Armijo AlexandraMorkmued SupawichAhumada José TomásKharouf Najide Feraudy YvanGogl GergoRiet FabriceNiederreither KarenLaporte JocelynBirling Marie ChristineSelloum MohammedHerault YannHernandez MagaliBloch-Zupan Agnès - Breast cancer ranks first in terms of mortality and incidence rates worldwide among women. The HER2+ molecular subtype is one of the most aggressive subtypes; its treatment includes neoadjuvant chemotherapy and the use of a HER2 antibody. Some patients develop resistance despite positive results obtained using this therapeutic strategy. - Source: PubMed
Publication date: 2022/10/21
Barrón-Gallardo Carlos AGarcia-Chagollán MarielMorán-Mendoza Andres JDelgadillo-Cristerna RaulMartínez-Silva María GVillaseñor-García María MAguilar-Lemarroy AdrianaJave-Suárez Luis F - The present study directly tested the crucial role of intestinal gastrin/CCKBR (cholecystokinin B receptor) in the treatment of salt-sensitive hypertension. - Source: PubMed
Publication date: 2022/06/08
Jiang XiaoliangLiu YunpengZhang Xin-YangLiu XueLiu XingWu XianxianJose Pedro ADuan ShunXu Fu-JianYang Zhiwei