Factor Nuclear(요인 핵)란 무엇입니까?
Factor Nuclear 요인 핵 - The transcription factor nuclear respiratory factor 1 (NRF1) has a novel and integral role in this neurodevelopmental process, being required for ncPRC1. [1] Transcription factor nuclear factor erythroid 2 p45-related factor 2 (Nrf2) and its main negative regulator, Kelch-like ECH associated protein 1 (Keap1), are at the interface between redox and intermediary metabolism. [2] The pan-inflammatory transcription factor nuclear factor-κB (NF-κB), the inflammasome sensor NLRP3, and the macrophage marker CD68 were all reduced in EV-treated animals. [3] The effects of all the treatments on the expression of phosphorylated cytokine tumor necrosis factor α (p-TNF-α) and phosphorylated transcription factor nuclear factor kappa B (p-NF-κB) expression in the cortex and hippocampus of the brains of treated rats were studied through enzyme linked immunosorbent assay (ELISA) and morphological differences and surviving neuronal number were recorded through hematoxylene and eosin (H&E) staining. [4] Therefore, the impact of genetic variations of receptors of the innate immune system—(Toll-like receptors (TLRs)) TLR2, TLR4, cluster of differentiation 14 (CD14), and the transcription factor nuclear factor-κΒ (NF-κB)—was investigated. [5] The expression levels of the atrial inflammation-associated factor nuclear factor κB (NF-κB) and its pathway were significantly altered in the atria of DM mice. [6] Further study demonstrated that Y-2 could reduce inflammatory response and oxidative stress by decreasing the levels of myeloperoxidase (MPO), ionized calcium-binding adaptor protein-1 (Iba-1), inflammatory cytokines and oxidative products, inhibit transcription factor nuclear factor-κB (NF-κB) activation, cyclooxygenase-2 (COX-2) and matrix metallopeptidase 9 (MMP-9) expression in brain tissue around in the core regions of hematoma. [7] Mechanistically, Bortezomib pretreatment significantly promoted nuclear translocation of transcriptional factor nuclear factor erythroid 2-related factor 2(Nrf2) and Heme Oxygenase 1(HO-1) expression. [8] Differentially methylated regions (DMRs) were functionally varied, including near transcription factor nuclear transcription factor Y subunit alpha (NFYA), receptor tyrosine kinase DDR1, RING finger ubiquitin ligase (RNF5), acetyltransferase AGPAT1, and vault RNA VTRNA2-1. [9] The experimental anti-leukemic drug parthenolide (PTL) acts by inhibiting transcription factor nuclear kappa B ( NFκB ) , activating p53 and increasing reactive oxygen species (ROS) in leukemic cells. [10] The transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2) plays a key role in cancer progression and is tightly regulated by the proteasome pathway. [11] The transcription factor nuclear factor-kB, that regulates many biological processes, was translocated from the cytoplasm to the nucleus in the absence of FH. [12] This is followed by precisely regulated cytosolic calcium (Ca2+cyt) oscillations, which stimulate the nuclear translocation of the transcription factor nuclear factor of activated T-cells (NFAT) and therefore mediate specific immunological modulations. [13] LPS-boosted activity of transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) of differentiated THP-1 reporter gene cells was marginally inhibited by Cy3glc. [14] The transcription factor nuclear factor-kappa B (NF-κB) plays a vital role in the inflammatory response following viral infections. [15] Transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), a detoxifying master transcription factor, is expressed mainly in astrocytes and activates the gene expression of various phase II drug-metabolizing enzymes or antioxidants including GSH-related molecules and metallothionein by binding to the antioxidant response element (ARE) of these genes. [16] This was accompanied by increased expression of the TLR adaptor protein myeloid differentiation primary response 88 (MyD88), activation of the proinflammatory nuclear transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), and downstream induction of proinflammatory cytokines, chemokines, and their corresponding receptors. [17] The transcription factor nuclear factor-kappa B (NF-κB) is critically involved in inflammation and cancer development. [18] The transcription factor Nuclear factor erythroid 2-related factor 2 (Nrf2), which regulates the expression of a great number of antioxidant and/or defense proteins, has been pointed as a potential pharmacological target involved in the mitigation of deleterious oxidative events taking place at the ischemic cascade. [19] As a major regulator of antioxidant responses, the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) has recently attracted much interest. [20] The transcription factor nuclear factor kappa B (NF-κB) and its dysregulation has a major impact on gastric carcinogenesis due to the regulation of cytokines/chemokines, growth factors, anti-apoptotic factors, cell cycle regulators, and metalloproteinases. [21] Inhibition of the enzyme heme oxygenase-1 (HO-1) or silencing of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) suppressed the AST-promoted cellular and mitochondrial protection. [22] Here we provide evidence that metformin induces accumulation of ROS by inhibiting the expression of a core antioxidant transcription factor nuclear factor erythroid 2 like 1 (NFE2L1/Nrf1) in human hepatocellular carcinoma HepG2 cells. [23] The transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) is a master controller of these functions, and its overall activity is compromised during aging and in these diseases. [24] Concentrations within 20–60 µM dose-dependently suppressed the LPS-induced expression, phosphorylation, and nuclear translocation of the inflammatory transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). [25] The transcription factor nuclear factor (erythroid-2)-related factor 2 (Nrf2) can principally serve a mode of protection for both the normal cells and cancer cells from cellular stress, and elevates cancer cell survival. [26] This regulation of cytokine secretion by H-P resulted in decreasing the expression level of the transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) in treated cells. [27] Mechanically, transcription factor nuclear factor‐κB (NF‐κB) selectively binds with κB element in the promoter of miR‐122 to accelerate gene transcription. [28] The ligand-sensing transcription factor nuclear receptor related 1 (Nurr1) evolves as an appealing target to treat neurodegenerative diseases. [29] Activation of RAGE by AGEs causes upregulation of the transcription factor nuclear factor-κB and its target genes. [30] The goals of the current study are to examine the extent and mechanisms of apoptosis in cholestatic liver injury and to explore the role of the transcription factor nuclear factor-kappa B (NFB) in protection against bile acid-induced apoptosis. [31] Using an inducible piggyBac (PB) transposon mutagenesis screen, we have shown that overexpression of the transcription factor nuclear factor IB (NFIB) alone is sufficient to enhance primary mammary tumour growth and lung metastatic colonization. [32] Finally, resveratrol attenuated the binding activity of the transcription factor nuclear factor-κB in WPMY-1 cells, and accelerated apoptotic cell death via intrinsic cascade pathway. [33] The expression of the pro‐inflammatory cytokines interleukin (IL)‐1β and tumour necrosis factor (TNF)‐α, the pro‐inflammatory transcription factor nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB), and inflammasome components (NLRP3, caspase‐1 and ASC) in CNP and BPH tissues was reduced by QLX addition. [34] This gene is responsible for the natural immune response and transcription factor nuclear factor kß (NFkß) activation in apoptosis. [35] It was previously reported that the loss of the transcription factor nuclear factor I/X (NFIX) gene in mice impaired endochondral ossification and mineralization in bone. [36] Among them, the transcription factor Nuclear Factor-Y subunit C (MdNF-YC2) functions as a promoter of flowering in Arabidopsis by activating LEAFY (LFY) and APETALA1 (AP1) expression. [37] Ca2+ nanodomains arising from store-operated Orai1 Ca2+ channels stimulate the protein phosphatase calcineurin to activate the transcription factor nuclear factor of activated T cells (NFAT). [38] Previously, we identified several ICPs, including programmed death-ligand 1 (PD-L1), tryptophan 2,3-dioxygenase 2 (TDO2), indoleamine 2, 3-dioxygenase 1 (IDO1) and growth differentiation factor 15 (GDF15), that were developmentally upregulated by transcription factor nuclear factor erythroid 2-related factor 2 (NRF2/NFE2L2) in human fetal lung epithelial cells during differentiation in culture. [39] We hypothesized that reactive oxygen species (ROS) and the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2),which is an important regulator of cellular redox homeostasis, are plausible elements. [40] The transcription factor nuclear factor kappa-B (NF-ĸB) has been suggested as a potential therapeutic target in IPF and therefore the aim of this study was to investigate the efficacy of ACT001, an NF-ĸB inhibitor, on primary fibroblasts derived from patients with and without IPF. [41] Treatments currently under investigation include inhibitors of kallikrein 5, cathelicidins, drugs activating the transcription factor nuclear factor erythroid-derived 2-like 2, and gene therapy using autologous keratinocytes induced with a lentiviral vector encoding SPINK5. [42] Inhibition of heme oxygenase-1 (HO-1) or silencing of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) blocked the T-I-promoted mitochondrial protection and anti-inflammatory action. [43] We also observed that apoptosis-inducing factor nuclear translocation and PAR accumulation were associated with the necroptosis signal. [44] Hyperglycemia during skin aging not only causes oxidative damage to cellular macromolecules, like dermal collagen, but also modulates the activation of transcription factor nuclear factor kappa B (NF-kB). [45] The transcription factor nuclear factor erythroid 2‐related factor 2 (Nrf2) regulates an array of cytoprotective genes, yet studies in transgenic mice have led to conflicting reports on its role in liver regeneration. [46] SFN is a potent activator of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), which is a master regulator of the mammalian redox biology. [47] HO-1 expression is primarily regulated at the transcriptional level through transcriptional factor nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2), specificity protein 1 (Sp1), transcriptional repressor BTB-and-CNC homology 1 (Bach1), and epigenetic regulation. [48] The promyogenic factor nuclear factor of activated T-cells 5 (NFAT5) is virtually present in all cells, responding to hyperosmolar or pro-inflammatory stress. [49] Besides, inhibition of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway, as well as silencing of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), suppressed the CA-stimulated protection and the synthesis of GSH. [50]전사 인자 핵 호흡 인자 1(NRF1)은 ncPRC1에 필요한 이 신경 발달 과정에서 새롭고 필수적인 역할을 합니다. [1] 전사 인자 핵 인자 적혈구계 2 p45 관련 인자 2(Nrf2)와 주요 음성 조절자인 Kelch-like ECH 관련 단백질 1(Keap1)은 산화환원과 중간 대사 사이의 경계면에 있습니다. [2] 범-염증 전사 인자 핵 인자-κB(NF-κB), 인플라마좀 센서 NLRP3 및 대식세포 마커 CD68은 EV 처리 동물에서 모두 감소했습니다. [3] 처리된 쥐의 뇌 피질과 해마에서 인산화된 사이토카인 종양 괴사 인자 α(p-TNF-α) 및 인산화된 전사 인자 핵 인자 카파 B(p-NF-κB) 발현에 대한 모든 처리의 효과 효소 결합 면역흡착 분석법(ELISA)을 통해 연구하고 형태학적 차이와 생존 신경 세포 수를 헤마토자일렌 및 에오신(H&E) 염색을 통해 기록했습니다. [4] nan [5] nan [6] nan [7] 기계적으로, Bortezomib 전처리는 전사 인자 핵 인자 erythroid 2 관련 인자 2(Nrf2) 및 Heme Oxygenase 1(HO-1) 발현의 핵 전위를 크게 촉진했습니다. [8] nan [9] 실험적인 항백혈병 약물 파르테놀라이드(PTL)는 전사 인자 핵 카파 B(NFκB)를 억제하고, p53을 활성화하고, 백혈병 세포에서 활성 산소 종(ROS)을 증가시켜 작용합니다. [10] 전사 인자 핵 인자(적혈구 유래 2)-유사 2(NRF2)는 암 진행에서 핵심적인 역할을 하며 프로테아좀 경로에 의해 엄격하게 조절됩니다. [11] nan [12] nan [13] 분화된 THP-1 리포터 유전자 세포의 활성화된 B 세포(NF-κB)의 전사 인자 핵 인자 카파-경쇄 인핸서의 LPS-부스트 활성은 Cy3glc에 의해 미미하게 억제되었다. [14] nan [15] nan [16] 이것은 TLR 어댑터 단백질 골수 분화 1차 반응 88(MyD88)의 증가된 발현, 활성화된 B 세포의 전염증성 핵 전사 인자 핵 인자 카파-경쇄 증강 인자(NFκB)의 활성화 및 전염증성 사이토카인의 다운스트림 유도를 동반했습니다. , 케모카인 및 해당 수용체. [17] nan [18] nan [19] nan [20] nan [21] 효소 헴 옥시게나제-1(HO-1)의 억제 또는 전사 인자 핵 인자 적혈구계 2 관련 인자 2(Nrf2)의 억제는 AST 촉진 세포 및 미토콘드리아 보호를 억제했습니다. [22] nan [23] nan [24] nan [25] nan [26] nan [27] nan [28] 리간드 감지 전사 인자 핵 수용체 관련 1(Nurr1)은 신경퇴행성 질환을 치료하는 매력적인 표적으로 진화하고 있습니다. [29] nan [30] nan [31] nan [32] nan [33] nan [34] nan [35] nan [36] nan [37] nan [38] nan [39] nan [40] nan [41] 현재 연구 중인 치료법에는 칼리크레인 5 억제제, 카텔리시딘, 전사인자 핵인자 적혈구계 2-like 2를 활성화시키는 약물, SPINK5를 코딩하는 렌티바이러스 벡터로 유도된 자가 케라티노사이트를 이용한 유전자 치료 등이 있다. [42] 헴 옥시게나제-1(HO-1)의 억제 또는 전사 인자 핵 인자 적혈구계 2 관련 인자 2(Nrf2)의 억제는 T-I-촉진 미토콘드리아 보호 및 항염증 작용을 차단합니다. [43] 우리는 또한 세포 사멸 유도 인자 핵 전위 및 PAR 축적이 괴사 신호와 관련이 있음을 관찰했습니다. [44] nan [45] nan [46] nan [47] HO-1 발현은 주로 전사 인자 핵 인자 적혈구계 2(NF-E2) 관련 인자 2(Nrf2), 특이성 단백질 1(Sp1), 전사 억제인자 BTB-및-CNC 상동성 1(Bach1)을 통해 전사 수준에서 조절됩니다 , 그리고 후생적 조절. [48] nan [49] nan [50]
factor erythroid 2 인자 적혈구 2
Transcription factor nuclear factor erythroid 2 p45-related factor 2 (Nrf2) and its main negative regulator, Kelch-like ECH associated protein 1 (Keap1), are at the interface between redox and intermediary metabolism. [1] Mechanistically, Bortezomib pretreatment significantly promoted nuclear translocation of transcriptional factor nuclear factor erythroid 2-related factor 2(Nrf2) and Heme Oxygenase 1(HO-1) expression. [2] Transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), a detoxifying master transcription factor, is expressed mainly in astrocytes and activates the gene expression of various phase II drug-metabolizing enzymes or antioxidants including GSH-related molecules and metallothionein by binding to the antioxidant response element (ARE) of these genes. [3] The transcription factor Nuclear factor erythroid 2-related factor 2 (Nrf2), which regulates the expression of a great number of antioxidant and/or defense proteins, has been pointed as a potential pharmacological target involved in the mitigation of deleterious oxidative events taking place at the ischemic cascade. [4] As a major regulator of antioxidant responses, the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) has recently attracted much interest. [5] Here we provide evidence that metformin induces accumulation of ROS by inhibiting the expression of a core antioxidant transcription factor nuclear factor erythroid 2 like 1 (NFE2L1/Nrf1) in human hepatocellular carcinoma HepG2 cells. [6] The transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) is a master controller of these functions, and its overall activity is compromised during aging and in these diseases. [7] The transcription factor nuclear factor (erythroid-2)-related factor 2 (Nrf2) can principally serve a mode of protection for both the normal cells and cancer cells from cellular stress, and elevates cancer cell survival. [8] Previously, we identified several ICPs, including programmed death-ligand 1 (PD-L1), tryptophan 2,3-dioxygenase 2 (TDO2), indoleamine 2, 3-dioxygenase 1 (IDO1) and growth differentiation factor 15 (GDF15), that were developmentally upregulated by transcription factor nuclear factor erythroid 2-related factor 2 (NRF2/NFE2L2) in human fetal lung epithelial cells during differentiation in culture. [9] We hypothesized that reactive oxygen species (ROS) and the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2),which is an important regulator of cellular redox homeostasis, are plausible elements. [10] SFN is a potent activator of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), which is a master regulator of the mammalian redox biology. [11] HO-1 expression is primarily regulated at the transcriptional level through transcriptional factor nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2), specificity protein 1 (Sp1), transcriptional repressor BTB-and-CNC homology 1 (Bach1), and epigenetic regulation. [12] Besides, inhibition of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway, as well as silencing of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), suppressed the CA-stimulated protection and the synthesis of GSH. [13] The transcription factor nuclear factor-erythroid 2-related factor 2 (Nrf2) is widely recognized as a master regulator of the cellular stress response by facilitating the transcription of cytoprotective genes. [14] Sulforaphane potently induces transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated expression of detoxification, anti-oxidation, and immune system-modulating enzymes, and possibly acts as an anti-carcinogenic agent. [15] The transcription factor nuclear factor erythroid 2-like 2 (NEF2L2; NRF2) plays crucial roles in the defense system against electrophilic or oxidative stress by upregulating an array of genes encoding antioxidant proteins, electrophile/reactive oxygen species (ROS) detoxifying enzymes, and drug efflux transporters. [16] Transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) plays a crucial role in regulating the expression of genes participating in cellular defense mechanisms against oxidative or xenobiotic insults. [17] The phytochemical and bioactive agent sulforaphane (SFN) has nutrigenomic potential in activating the expression of several cellular protective genes via the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2). [18] In this study, xanthohumol prevented tert-butyl hydroperoxide-induced loss of cell viability in human corneal epithelial (HCE-T) cells in a dose-dependent manner and resulted in a significant increase in expression of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), the master regulator of phase II endogenous antioxidant enzymes. [19] We particularly focused on the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2), the first line of antioxidant defense in cells, and on the glutathione (GSH) system, an index of reactive oxygen species (ROS) detoxification ability. [20] The induction of these genes is tightly regulated by transcription factor nuclear factor erythroid 2 p45–related factor 2 (NRF2), a potential target of microRNA (miR)-144. [21] Redox balance in the heart and brain is controlled, in part, by antioxidant proteins regulated by the transcription factor Nuclear factor erythroid 2-related factor 2 (Nrf2), which is reduced in the heart failure state. [22] Recent studies have demonstrated that the transcription factor nuclear factor-erythroid 2-related factor 2 (Nrf2) and its key negative regulator Kelch-like ECH-associated protein 1 (Keap1) are dysregulated in PC and the Keap1-Nrf2 pathway is an emerging target for PC prevention and therapy. [23]전사 인자 핵 인자 적혈구계 2 p45 관련 인자 2(Nrf2)와 주요 음성 조절자인 Kelch-like ECH 관련 단백질 1(Keap1)은 산화환원과 중간 대사 사이의 경계면에 있습니다. [1] 기계적으로, Bortezomib 전처리는 전사 인자 핵 인자 erythroid 2 관련 인자 2(Nrf2) 및 Heme Oxygenase 1(HO-1) 발현의 핵 전위를 크게 촉진했습니다. [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] HO-1 발현은 주로 전사 인자 핵 인자 적혈구계 2(NF-E2) 관련 인자 2(Nrf2), 특이성 단백질 1(Sp1), 전사 억제인자 BTB-및-CNC 상동성 1(Bach1)을 통해 전사 수준에서 조절됩니다 , 그리고 후생적 조절. [12] nan [13] nan [14] nan [15] nan [16] nan [17] nan [18] nan [19] nan [20] nan [21] nan [22] nan [23]