| CLIC4 Regulates Endothelial Barrier Control by Mediating PAR1 Signaling via RhoA. | CLIC4 Regulates Endothelial Barrier Control by Mediating PAR1 Signaling via RhoA.
Kleinjan ML, Mao Y, Naiche LA, Joshi JC, Gupta A, Jesse JJ, Shaye DD, Mehta D, Kitajewski J., | 09/6/2023 |
| The oxidoreductase CLIC4 is required to maintain mitochondrial function and resistance to exogenous oxidants in breast cancer cells. | The oxidoreductase CLIC4 is required to maintain mitochondrial function and resistance to exogenous oxidants in breast cancer cells.
Al Khamici H, Sanchez VC, Yan H, Cataisson C, Michalowski AM, Yang HH, Li L, Lee MP, Huang J, Yuspa SH., Free PMC Article | 10/22/2022 |
| Chloride intracellular channel 4 (CLIC4) expression profile in the mouse medial prefrontal cortex and its regulation by ethanol. | Chloride intracellular channel 4 (CLIC4) expression profile in the mouse medial prefrontal cortex and its regulation by ethanol.
Bogenpohl JW, Weston RM, Foreman TN, Kitchen KE, Miles MF., Free PMC Article | 03/12/2022 |
| Retinal pigment epithelium-specific CLIC4 mutant is a mouse model of dry age-related macular degeneration. | Retinal pigment epithelium-specific CLIC4 mutant is a mouse model of dry age-related macular degeneration.
Chuang JZ, Yang N, Nakajima N, Otsu W, Fu C, Yang HH, Lee MP, Akbar AF, Badea TC, Guo Z, Nuruzzaman A, Hsu KS, Dunaief JL, Sung CH., Free PMC Article | 02/19/2022 |
| CLIC1 and CLIC4 mediate endothelial S1P receptor signaling to facilitate Rac1 and RhoA activity and function. | CLIC1 and CLIC4 mediate endothelial S1P receptor signaling to facilitate Rac1 and RhoA activity and function.
Mao Y, Kleinjan ML, Jilishitz I, Swaminathan B, Obinata H, Komarova YA, Bayless KJ, Hla T, Kitajewski JK., Free PMC Article | 01/22/2022 |
| Results indicate CLICs (CLIC1, CLIC4 and CLIC5)-dependent chloride efflux as an essential and proximal upstream event for NLRP3 activation. | CLICs-dependent chloride efflux is an essential and proximal upstream event for NLRP3 inflammasome activation.
Tang T, Lang X, Xu C, Wang X, Gong T, Yang Y, Cui J, Bai L, Wang J, Jiang W, Zhou R., Free PMC Article | 12/9/2017 |
| Data, including data from studies in primary cells from knockout mice, suggest Clic1 and Clic4 participate in signaling interleukin 1beta secretion and in activation of Nlrp3 inflammasomes; in LPS macrophage activation, Clic1 and Clic4 are translocated to nucleus/cell membranes. (Clic1 = chloride intracellular channel 1; Clic4 = chloride intracellular channel 4, mitochondrial; Nlrp3 = NLR family pyrin domain containing 3) | The intracellular chloride channel proteins CLIC1 and CLIC4 induce IL-1β transcription and activate the NLRP3 inflammasome.
Domingo-Fernández R, Coll RC, Kearney J, Breit S, O'Neill LAJ., Free PMC Article | 08/12/2017 |
| study reports an alternately-spliced form of Smad7, Smad7Delta, that is induced by TGF-beta and CLIC4, is a dominant inhibitor of Smad7 and enhances TGF-beta signaling | Elevating CLIC4 in Multiple Cell Types Reveals a TGF- Dependent Induction of a Dominant Negative Smad7 Splice Variant.
Shukla A, Yang Y, Madanikia S, Ho Y, Li M, Sanchez V, Cataisson C, Huang J, Yuspa SH., Free PMC Article | 07/29/2017 |
| The findings indicate that CLIC4/CLIC5A-mediated ERM activation is required for maintenance of the glomerular capillary architecture. | Both CLIC4 and CLIC5A activate ERM proteins in glomerular endothelium.
Tavasoli M, Al-Momany A, Wang X, Li L, Edwards JC, Ballermann BJ. | 07/8/2017 |
| CLIC4 is not required for collaterogenesis but is essential for perinatal maturation of nascent collaterals through a mechanism that supports VEGF signaling. | Chloride intracellular channel 4 is required for maturation of the cerebral collateral circulation.
Lucitti JL, Tarte NJ, Faber JE., Free PMC Article | 01/2/2016 |
| However, the absence of CLIC4 has no significant impact on the extent of functional recovery or fibrosis following acute injury. | Absence of chloride intracellular channel 4 (CLIC4) predisposes to acute kidney injury but has minimal impact on recovery.
Edwards JC, Bruno J, Key P, Cheng YW., Free PMC Article | 12/20/2014 |
| Data suggest that compartmentalized expression of chloride intracellular channel 4 (CLIC4) in specific adult tissues and cells provides a focus to explore potential functions of this protein. | Detection of differential fetal and adult expression of chloride intracellular channel 4 (CLIC4) protein by analysis of a green fluorescent protein knock-in mouse line.
Padmakumar V, Masiuk KE, Luger D, Lee C, Coppola V, Tessarollo L, Hoover SB, Karavanova I, Buonanno A, Simpson RM, Yuspa SH., Free PMC Article | 10/4/2014 |
| Increased CLIC4 expression is an early manifestation and mediator of endothelial dysfunction in pulmonary hypertension. | Aberrant chloride intracellular channel 4 expression contributes to endothelial dysfunction in pulmonary arterial hypertension.
Wojciak-Stothard B, Abdul-Salam VB, Lao KH, Tsang H, Irwin DC, Lisk C, Loomis Z, Stenmark KR, Edwards JC, Yuspa SH, Howard LS, Edwards RJ, Rhodes CJ, Gibbs JS, Wharton J, Zhao L, Wilkins MR., Free PMC Article | 06/28/2014 |
| These results indicate that CLIC4 participates in skin healing and corneal wound reepithelialization through enhancement of epithelial migration by a mechanism that may involve a compromised TGF-beta pathway. | Spontaneous skin erosions and reduced skin and corneal wound healing characterize CLIC4(NULL) mice.
Padmakumar VC, Speer K, Pal-Ghosh S, Masiuk KE, Ryscavage A, Dengler SL, Hwang S, Edwards JC, Coppola V, Tessarollo L, Stepp MA, Yuspa SH., Free PMC Article | 11/3/2012 |
| Data suggest that iNOS-induced nuclear CLIC4 is an essential part of the macrophage deactivation program. | Inducible NOS-induced chloride intracellular channel 4 (CLIC4) nuclear translocation regulates macrophage deactivation.
Malik M, Jividen K, Padmakumar VC, Cataisson C, Li L, Lee J, Howard OM, Yuspa SH., Free PMC Article | 07/14/2012 |
| CLIC4 is required for an optimal macrophage response to diverse pathogens. CLIC4-null these findings suggest that CLIC4 is an LPS-induced product that can serve as a positive regulator of LPS signaling | Role of CLIC4 in the host innate responses to bacterial lipopolysaccharide.
He G, Ma Y, Chou SY, Li H, Yang C, Chuang JZ, Sung CH, Ding A., Free PMC Article | 06/25/2011 |
| S-nitrosylation governs CLIC4 structure, its association with protein partners, and thus its intracellular distribution | S-nitrosylation regulates nuclear translocation of chloride intracellular channel protein CLIC4.
Malik M, Shukla A, Amin P, Niedelman W, Lee J, Jividen K, Phang JM, Ding J, Suh KS, Curmi PM, Yuspa SH., Free PMC Article | 09/20/2010 |
| CLIC4 specifies native collateral formation, exerting influences upstream of hypoxia-inducible factor-1alpha-VEGF signaling | Chloride intracellular channel-4 is a determinant of native collateral formation in skeletal muscle and brain.
Chalothorn D, Zhang H, Smith JE, Edwards JC, Faber JE., Free PMC Article | 01/21/2010 |
| These results newly identify Schnurri-2 and CLIC4 as modifiers of TGF-beta signalling through their stabilization of p-Smad2 and 3 in the nucleus. | TGF-beta signalling is regulated by Schnurri-2-dependent nuclear translocation of CLIC4 and consequent stabilization of phospho-Smad2 and 3.
Shukla A, Malik M, Cataisson C, Ho Y, Friesen T, Suh KS, Yuspa SH., Free PMC Article | 01/21/2010 |
| CLIC4 plays a critical role in angiogenesis by supporting acidification of vacuoles along the cell-hollowing tubulogenic pathway. | Chloride intracellular channel protein-4 functions in angiogenesis by supporting acidification of vacuoles along the intracellular tubulogenic pathway.
Ulmasov B, Bruno J, Gordon N, Hartnett ME, Edwards JC., Free PMC Article | 01/21/2010 |
| mtCLIC is involved in mitochondrial membrane potential generation in mitochondrial DNA-depleted cells. | mtCLIC is up-regulated and maintains a mitochondrial membrane potential in mtDNA-depleted L929 cells.
Arnould T, Mercy L, Houbion A, Vankoningsloo S, Renard P, Pascal T, Ninane N, Demazy C, Raes M. | 01/21/2010 |
| mtCLIC/CLIC4, an organellular chloride channel protein, is increased by DNA damage and participates in the apoptotic response to p53. | mtCLIC/CLIC4, an organellular chloride channel protein, is increased by DNA damage and participates in the apoptotic response to p53.
Fernández-Salas E, Suh KS, Speransky VV, Bowers WL, Levy JM, Adams T, Pathak KR, Edwards LE, Hayes DD, Cheng C, Steven AC, Weinberg WC, Yuspa SH., Free PMC Article | 01/21/2010 |
| CLIC4 nuclear translocation is an integral part of the cellular response to stress and may contribute to the initiation of nuclear alterations that are associated with apoptosis. | The organellular chloride channel protein CLIC4/mtCLIC translocates to the nucleus in response to cellular stress and accelerates apoptosis.
Suh KS, Mutoh M, Nagashima K, Fernandez-Salas E, Edwards LE, Hayes DD, Crutchley JM, Marin KG, Dumont RA, Levy JM, Cheng C, Garfield S, Yuspa SH. | 01/21/2010 |