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• W2786103310 endingPage "273" @default.
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• W2786103310 abstract "Ca2+ homeostasis alterations lead to defects in cell cycle progression. inositol 1,4,5-trisphosphate (IP3) receptors are a target of oncogenes and tumor suppressors. Ca2+ signaling has an important but still controversial role in inflammasome activation. Ca2+ signaling has a key role in synaptic activity and plasticity as well as in neurodegeneration. The mitochondrial calcium uniporter (MCU) is not essential for homeostatic cardiac function. Calcium (Ca2+) is considered one of the most-important biological cations, because it is implicated in cell physiopathology and cell fate through a finely tuned signaling system. In support of this notion, Ca2+ is the primary driver of cell proliferation and cell growth; however, it is also intimately linked to cell death. Functional abnormalities or mutations in proteins that mediate Ca2+ homeostasis usually lead to a plethora of diseases and pathogenic states, including cancer, heart failure, diabetes, and neurodegenerative disease. In this review, we examine recent discoveries in the highly localized nature of Ca2+-dependent signal transduction and its roles in cell fate, inflammasome activation, and synaptic transmission. Calcium (Ca2+) is considered one of the most-important biological cations, because it is implicated in cell physiopathology and cell fate through a finely tuned signaling system. In support of this notion, Ca2+ is the primary driver of cell proliferation and cell growth; however, it is also intimately linked to cell death. Functional abnormalities or mutations in proteins that mediate Ca2+ homeostasis usually lead to a plethora of diseases and pathogenic states, including cancer, heart failure, diabetes, and neurodegenerative disease. In this review, we examine recent discoveries in the highly localized nature of Ca2+-dependent signal transduction and its roles in cell fate, inflammasome activation, and synaptic transmission. contain a protein motif comprising approximately 50 amino acids that functions as a protein–protein interaction site. F-box proteins are substrate receptors of the SKP1-Cullin 1-F-box protein (SCF) E3 ubiquitin ligase and have important roles in several physiological processes and activities. In humans, there are 69 SCF ligases, each utilizing a different F-box protein subunit. F-box proteins are classified into three subfamilies (FBXW, FBXL, and FBXO) depending on the presence of specific domains other than the F-box motif, which is important for binding to the SKP1 adaptor. Importantly, the FBXL subfamily is characterized by the presence of leucine-rich repeats. multiprotein signaling complexes that operate as platforms for the activation of inflammatory caspases and the maturation of a set of proinflammatory cytokines. Inflammasome formation is triggered by a range of substances that emerge during infection, tissue damage, or metabolic imbalances. Once the protein complexes form, inflammasomes activate caspase-1, which proteolytically activates the proinflammatory cytokines interleukin-1β and interleukin-18. In addition, inflammasome activation causes a rapid, proinflammatory form of cell death termed pyroptosis. located at the inner mitochondrial membrane and includes the channel-forming subunit MCU (also known as CCDC109A) and MCU regulatory subunit b (MCUb; also known as CCDC109B). EMRE (also known as C22orf32) and MICU1 (previously known as CBARA1 and EFHA3) are essential MCU regulators. Other important regulators are MICU2 (also known as EFHA1) and MICU3 (also known as EFHA2). a pump that transports Ca2+ from the cytosol to the SR/ER and Golgi apparatus. The different isoforms (SERCA1, SERCA2a, SERCA2b, and SERCA3) are species and tissue specific. Ca2+ homeostasis and SERCA2 activity represent a nodal point linking vascular remodeling and cell survival. a major route of Ca2+ entry in nonexcitable cells. SOCE is mediated by the STIM and ORAI proteins and has recently been implicated in cancer cell proliferation, metastasis, and tumor neovascularization, as well as in antitumor immunity. Enhanced expression of ORAI1 and STIM1 as well as enhanced SOCE have been reported in therapy-resistant ovarian carcinoma cells and in colorectal, cervical, liver, lung, and clear cell renal cancers." @default.
• W2786103310 created "2018-02-23" @default.
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• W2786103310 creator A5087378098 @default.
• W2786103310 date "2018-04-01" @default.
• W2786103310 modified "2023-10-01" @default.
• W2786103310 title "Calcium Dynamics as a Machine for Decoding Signals" @default.
• W2786103310 cites W1486654044 @default.
• W2786103310 cites W1561041814 @default.
• W2786103310 cites W1622243645 @default.
• W2786103310 cites W1859128422 @default.
• W2786103310 cites W1895235630 @default.
• W2786103310 cites W1973109734 @default.
• W2786103310 cites W1979385451 @default.
• W2786103310 cites W1983181941 @default.
• W2786103310 cites W1987329700 @default.
• W2786103310 cites W1990004900 @default.
• W2786103310 cites W1994473516 @default.
• W2786103310 cites W2000115025 @default.
• W2786103310 cites W2000117406 @default.
• W2786103310 cites W2001367960 @default.
• W2786103310 cites W2004325585 @default.
• W2786103310 cites W2005216847 @default.
• W2786103310 cites W2021592710 @default.
• W2786103310 cites W2025102008 @default.
• W2786103310 cites W2037600884 @default.
• W2786103310 cites W2043751060 @default.
• W2786103310 cites W2044496334 @default.
• W2786103310 cites W2054723193 @default.
• W2786103310 cites W2056633265 @default.
• W2786103310 cites W2070658923 @default.
• W2786103310 cites W2071517838 @default.
• W2786103310 cites W2074185046 @default.
• W2786103310 cites W2079761894 @default.
• W2786103310 cites W2080308068 @default.
• W2786103310 cites W2084281549 @default.
• W2786103310 cites W2101826917 @default.
• W2786103310 cites W2110962130 @default.
• W2786103310 cites W2115021528 @default.
• W2786103310 cites W2117407594 @default.
• W2786103310 cites W2117977069 @default.
• W2786103310 cites W2121711825 @default.
• W2786103310 cites W2126785984 @default.
• W2786103310 cites W2128767149 @default.
• W2786103310 cites W2135149951 @default.
• W2786103310 cites W2140523553 @default.
• W2786103310 cites W2145563296 @default.
• W2786103310 cites W2154150494 @default.
• W2786103310 cites W2155353396 @default.
• W2786103310 cites W2165722259 @default.
• W2786103310 cites W2223504418 @default.
• W2786103310 cites W2274199511 @default.
• W2786103310 cites W2276801987 @default.
• W2786103310 cites W2291641483 @default.
• W2786103310 cites W2294335173 @default.
• W2786103310 cites W2326752152 @default.
• W2786103310 cites W2338118586 @default.
• W2786103310 cites W2363363069 @default.
• W2786103310 cites W2396452471 @default.
• W2786103310 cites W2412698309 @default.
• W2786103310 cites W2420066879 @default.
• W2786103310 cites W2498411827 @default.
• W2786103310 cites W2504803702 @default.
• W2786103310 cites W2506140674 @default.
• W2786103310 cites W2514431030 @default.
• W2786103310 cites W2518040164 @default.
• W2786103310 cites W2523345792 @default.
• W2786103310 cites W2527503499 @default.
• W2786103310 cites W2549436143 @default.
• W2786103310 cites W2549673184 @default.
• W2786103310 cites W2552594066 @default.
• W2786103310 cites W2559652912 @default.
• W2786103310 cites W2560077369 @default.
• W2786103310 cites W2571183123 @default.
• W2786103310 cites W2596115537 @default.
• W2786103310 cites W2609751917 @default.
• W2786103310 cites W2611851783 @default.
• W2786103310 cites W2613068463 @default.
• W2786103310 cites W2616955232 @default.
• W2786103310 cites W2619658153 @default.
• W2786103310 cites W2620432483 @default.
• W2786103310 cites W2624817404 @default.
• W2786103310 cites W2626999699 @default.
• W2786103310 cites W2627401075 @default.
• W2786103310 cites W2634604042 @default.
• W2786103310 cites W2671935597 @default.
• W2786103310 cites W2744604441 @default.
• W2786103310 cites W2761087981 @default.
• W2786103310 cites W4255760236 @default.
• W2786103310 doi "https://doi.org/10.1016/j.tcb.2018.01.002" @default.
• W2786103310 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29409699" @default.
• W2786103310 hasPublicationYear "2018" @default.
• W2786103310 type Work @default.
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• W2786103310 citedByCount "166" @default.

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