CLIC4
- Known as:
- CLIC4
- Catalog number:
- Y213684
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CLIC4
Related genes to: CLIC4
- Gene:
- CLIC4 NIH gene
- Name:
- chloride intracellular channel 4
- Previous symbol:
- -
- Synonyms:
- DKFZP566G223, CLIC4L, P64H1, H1, huH1, p64H1
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2000-10-31
- Date modifiied:
- 2016-10-05
Related products to: CLIC4
anti-CLIC4anti-CLIC4 (N-Terminus)anti-CLIC4 (N-Terminus)anti-CLIC4 (N-Terminus)anti-CLIC4, Goat polyclonal to CLIC4, Isotype , Host GoatAnti-CLIC4, Rabbit Polyclonal to CLIC4, Isotype , Host RabbitAntibodies: CLIC4 HOST: Goat Clonality: pAbAntibody to Chloride Intracellular Channel Protein 4 (CLIC4) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntibody to Chloride Intracellular Channel Protein 4 (CLIC4) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntibody to Chloride Intracellular Channel Protein 4 (CLIC4) Organism: Mus musculus (Mouse) Type: Polyclonal Source: RabbitAntibody to Chloride Intracellular Channel Protein 4 (CLIC4) Organism: Mus musculus (Mouse) Type: Polyclonal Source: RabbitAntibody to Chloride Intracellular Channel Protein 4 (CLIC4) Organism: Rattus norvegicus (Rat) Type: Polyclonal Source: RabbitAntibody to Chloride Intracellular Channel Protein 4 (CLIC4) Organism: Rattus norvegicus (Rat) Type: Polyclonal Source: RabbitAntigens CLIC4, 1-253aa, Human, His tag, E.coli, Recombinantapoptosis: CLIC4, 1-253aa, Human, His tag, E.coli Related articles to: CLIC4
- Membrane channels are central to bladder function, yet current understanding is shaped disproportionately by a few well-studied families such as TRPA1 and TRPV1. To provide a more balanced view, this review analyzed emerging human transcriptomic datasets to identify the channels most highly expressed in the urinary bladder and examined how they remodel in bladder outlet obstruction and denervation. Sixty-seven channels were prominently expressed at the mRNA level in GTEx bladder tissue, with correlation analyses and protein expression data assigning many to smooth muscle, urothelial, endothelial, or neuronal compartments. Several abundant channels remain largely unstudied in urological contexts, including , , and . Disease-associated remodeling revealed shared and model-specific patterns. Outlet obstruction produced marked upregulation of L-type Ca channel auxiliary subunits and robust changes in CLIC-family channels, whereas denervation induced broader channel downregulation not explained by nerve loss alone. Three channels, , and , were concordantly altered in both conditions, suggesting coordinated changes within interstitial cell networks and mechanotransductive pathways. These findings highlight a diverse and incompletely explored bladder "channel-ome." Expanding research beyond traditional targets may uncover new mechanisms underlying storage and voiding dysfunction and provide opportunities for therapeutic innovation in lower urinary tract disease. - Source: PubMed
Publication date: 2026/04/07
Swärd KarlAndersson Karl-ErikUvelius Bengt - Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by impaired memory and cognitive decline. The early stages of AD in mice present with neuropathy in the hippocampus. Excessive mitochondrial fragmentation and dysfunction are critical pathological features of AD. Chloride intracellular channel 4 (CLIC4) is involved in neuronal apoptosis and regulates mitochondrial functions. Glial maturation factor β (GMFβ) inhibits mitochondrial DNA replication and energy metabolism, causes mitochondrial dysfunction, and regulates apoptosis. Dynamic related protein 1 (DRP1), a key protein in mitochondrial division, exhibits increased activity when its Ser616 site is phosphorylated. However, the role of CLIC4 in Aβ-induced cognitive impairment through the modulation of GMFβ and p-DRP1 (Ser616) to induce mitochondrial dysfunction remains unclear. This study examined the role of CLIC4 in Aβ-induced cognitive impairment in AD mice, focusing on its regulation of GMFβ and p-DRP1 (Ser616) and the subsequent effects on mitochondrial hyperfission and dysfunction. Our findings demonstrate that overexpression of CLIC4 in the mouse hippocampus or in HT22 cells resulted in pathological changes analogous to those observed following Aβ exposure. These changes include elevated levels of GMFβ and p-DRP1 (Ser616) proteins, mitochondrial fission, and increased intracellular ROS production. Conversely, CLIC4 knockdown mitigated Aβ-induced neuronal damage. These findings indicate that CLIC4 may be crucial in Aβ-induced hippocampal neurological damage in mice by regulating GMFβ and DRP1 phosphorylation. - Source: PubMed
Publication date: 2026/04/02
Wang JiaoMao XinyuZheng RenjiGao HuiqingChen GangZhang YantongXu MengtingLin QichengNivar JohnTao Yuan-XiangSun MingyangCao HongZhang JiaQiangLi Jun - Rheumatoid arthritis (RA) is a chronic autoimmune disease driven by aberrant activation of fibroblast-like synoviocytes (FLS), which promote synovial inflammation, joint destruction, and disease progression through enhanced migration and invasion. While mitochondrial dysfunction and reactive oxygen species (ROS) contribute to FLS pathogenicity, the regulatory mechanisms remain unclear. This study investigates the role of chloride intracellular channel 5 (CLIC5) in RA synovium and FLS function. Bioinformatic analysis of bulk and single-cell RNA sequencing datasets revealed significantly reduced CLIC5 expression in RA synovial tissues compared to healthy or osteoarthritis controls, predominantly in fibroblast subsets. Lower CLIC5 levels correlated negatively with histological inflammation scores (CD3, CD20, CD138), serological markers (CRP, ESR), and disease activity indices (DAS28, joint counts), establishing CLIC5 downregulation as a feature of increased RA severity. Functional experiments in primary human FLS from healthy donors (HFLS-H) and RA patients (HFLS-RA) demonstrated that CLIC5B, the dominant isoform, maintains mitochondrial homeostasis. CLIC5 knockdown in HFLS-H cells induced mitochondrial depolarization and elevated ROS, while CLIC5B overexpression in HFLS-RA cells restored membrane potential and reduced ROS. CLIC5 deficiency promoted ROS-dependent translocation of CLIC1, CLIC4, and CLIC5B to the plasma membrane, enhancing FLS migration and invasion. Mechanistically, CLIC5B attenuated this by inhibiting CLIC1/CLIC4-mediated recruitment of PIP5K1A/C to the membrane, as confirmed by co-immunoprecipitation, immunofluorescence, and rescue assays where CLIC1/CLIC4 overexpression reversed CLIC5B's inhibitory effects. These findings identify CLIC5B as a negative regulator of pro-inflammatory FLS migration via the CLIC1/CLIC4-PIP5K1 axis, highlighting its potential as a therapeutic target for mitigating RA progression. - Source: PubMed
Publication date: 2026/03/24
Jiang FanZhou HongyiMao JingShen Haili - Chloride ions (Cl) regulate sperm physiology, influencing spermatogenesis, volume regulation, capacitation, and fertilization processes. They contribute to the maintenance of membrane potential and intracellular pH, both of which are critical for sperm motility and capacitation. Any deviation in Cl homeostasis causes impaired sperm function and male infertility. Although several Cl channels and transporters have been implicated in the Cl homeostasis and osmoregulation of sperm cells, the precise mechanisms and molecular components governing volume regulation during sperm development remain unclear. - Source: PubMed
Publication date: 2026/02/19
Loyo-Celis VeronicaSanghvi ShridharRaut Satish KCastillo Hiram Pachecode la Vega Beltran Jose LuisOrta GerardoMontanez-Barragan AlejandraPatel AaryanAmaro Victor Xavier AbonzaRao Shubha GururajaEdwards John CPartida-Sanchez SantiagoDarszon AlbertoGuerrero AdanSingh Harpreet - Chloride intracellular channels (CLICs) are important in cardiac cellular physiology. We aimed to determine the pathophysiological roles of CLICs in the heart. For this, we analyzed CLIC expression in cardiomyocytes in a mouse transverse aortic constriction (TAC) model to induce cardiac hypertrophy and failure, as well as in ventricular myocytes from patients with dilated cardiomyopathy (DCM) using single-cell RNA-sequencing. Single-ventricular myocytes were isolated from the left ventricular free wall of C57BL/6J mice after TAC (pre-TAC; Day 3 post-TAC; and Weeks 1, 2, 4, and 8 post-TAC). Gene expression was compared with data from sham controls. In mice, CLIC1 and CLIC4 expression significantly increased in Day 3 and Weeks 1, 2, and 4 post-TAC. CLIC5 expression showed an increase during all phases. Kyoto Encyclopedia of Genes and Genomes pathway analysis for genes associated with CLIC1, CLIC4, and CLIC5 revealed a strong association between focal adhesion activation and actin cytoskeleton regulation pathways linked to extracellular matrix (ECM) remodeling. CLIC1 and CLIC4 expression was also higher in cells from patients with DCM. Single-cell RNA-sequencing revealed the possible role of CLICs in myocardial ventricular remodeling linked to ECM, proposing their potential as therapeutic targets for cardiac hypertrophy and failure. - Source: PubMed
Oguri GakuNomura SeitaroNakajima TakafumiKikuchi HironobuObi SyotaroKomuro IsseiTakeda NorihikoToyoda ShigeruNakajima Toshiaki