Ask about this productRelated genes to: CLIC6 Blocking Peptide
- Gene:
- CLIC6 NIH gene
- Name:
- chloride intracellular channel 6
- Previous symbol:
- CLIC1L
- Synonyms:
- CLIC5
- Chromosome:
- 21q22.12
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2015-08-28
Related products to: CLIC6 Blocking Peptide
Related articles to: CLIC6 Blocking Peptide
- Disruption of cation homeostasis is increasingly recognized as a driver of breast cancer (BC) progression, yet a clinically actionable gene signature that quantifies this disturbance has been lacking. This study aims to systematically explore the value of cation homeostasis-related genes in the prognosis assessment of BC through bioinformatics analysis, construct and validate a prognostic model based on these genes, and integrate immune mechanism and drug sensitivity analyses to provide novel biomarkers and potential therapeutic targets for precise prognosis evaluation and individualized treatment of BC. - Source: PubMed
Publication date: 2026/04/29
Xu MingxingYe ZhihaoHong WeiminZhu LiquanHe ChaoqiYang ZhuotaoHu JunsiQian DaMeng XuliRen Zhuozhuo - Protein kinases are essential regulators of cellular signaling pathways and are deeply involved in breast cancer (BC) progression. This study aimed to identify BC molecular subtypes and construct a prognostic model based on kinase-related genes (KRGs). - Source: PubMed
Publication date: 2026/05/12
Ye ShuanglaiJi Shengwei - Nasopharyngeal carcinoma (NPC) is an Epstein-Barr virus-associated malignancy. Tumor-associated macrophages play a pivotal role in NPC development, but molecular mechanisms remain unclear. This study aimed to identify M1 macrophage-associated hub genes and investigate their biological functions in NPC via bioinformatics and experimental validation. - Source: PubMed
Publication date: 2026/05/06
Chen ZhuoLi MingxianGao PeiZhao Yulin - Exosomes can promote tumor development and regulate tumor immune responses, making them of significant value in Lung Adenocarcinoma (LUAD) management. In-depth exploration of exosome-related genes in LUAD is of great significance for expanding LUAD clinical treatment options. - Source: PubMed
Publication date: 2026/03/23
Miao YajunLi TaoLi RongLiu Yufei - Alzheimer's disease (AD), though defined as a cognitive disorder, often presents neuropsychiatric symptoms such as anxiety, depression, agitation and sleep disruptions years before the onset of frank memory impairment. An early pathological feature is the accumulation of hyperphosphorylated "pretangle" tau (pTau) in the locus coeruleus (LC), the brain's primary source of norepinephrine (NE). While clinical studies link LC pTau burden to behavioral abnormalities, causal mechanisms remain unclear. We developed a translationally-relevant mouse model that recapitulates the 'LC-first' phenomenon using cell type-specific viral expression of pathogenic P364S mutant human tau in LC neurons. Three months post-infusion, pTau accumulation induced anxiety- and compulsive-like behaviors and reduced sleep spindles without altering overall sleep architecture. Consistent with the behavioral phenotypes, electrophysiological recordings revealed significant increases in spontaneous and evoked firing of LC neurons, accompanied by robust astrocytic reactivity with no apparent cell death. Transcriptomic analysis identified upregulation of and downregulation of , suggesting changes in neuronal excitability. To further define molecular mechanisms, we developed a cell type-specific proteomics approach, which showed synaptic and metabolic alterations associated with LC-specific tau pathology. Early anxiety-like behaviors observed at 3 months diminished at later timepoints (6-9 months) and were replaced by anxiolytic characteristics. These findings demonstrate that pTau triggers phenotypes reflective of LC-NE hyperactivity in the early stages of AD pathogenesis, laying the foundation for the development of LC-based disease-modifying therapies to address neuropsychiatric manifestations. - Source: PubMed
Publication date: 2026/02/01
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