Rna Nuclear(르나 핵)란 무엇입니까?
Rna Nuclear 르나 핵 - Las dos especies pueden discriminarse también por las secuencias de su región espaciadora interna nuclear (nrITS). [1] After DNA extraction, 28S rRNA nuclear (710 bp) and cytochrome b (cytb) mitochondrial (520 bp) gene fragments were sequenced. [2]두 종은 또한 핵 내부 스페이서 영역(nrITS)의 서열에 의해 구별될 수 있습니다. [1] DNA 추출 후, 28S rRNA 핵(710 bp) 및 시토크롬 b(cytb) 미토콘드리아(520 bp) 유전자 단편을 시퀀싱했습니다. [2]
enriched abundant transcript 풍부한 풍부한 성적표
In the present study, we explored the roles and underlying mechanism of the lncRNA Nuclear enriched abundant transcript 1 (NEAT1) in ARDS. [1] Here, we profiled differences in epigenetic regulation between adipogenesis and osteogenesis and identified super-enhancer associated lncRNA nuclear-enriched abundant transcript 1 (NEAT1) as a key bone-fat switch in aged BMSCs. [2] This study aims to evaluate the predictive value of serum exosomal long noncoding RNA nuclear-enriched abundant transcript 1 (lncRNA NEAT1) for 90-day mortality of ACHBLF. [3] However, the mechanism underlying the influence of the lncRNA nuclear enriched abundant transcripts 1 (NEAT1) on CSF is still unknown. [4] Results LncRNA nuclear-enriched abundant transcript 1 (NEAT1) expression levels were decreased in the CML cell lines and PBMCs of CML patients. [5] Here, we investigated the role of lncRNA nuclear-enriched abundant transcript 1 (NEAT1) in ESCC via regulating microRNA 1299 (miR-1299) and matrix metalloproteinase 2 (MMP2). [6] LncRNA nuclear-enriched abundant transcript 1 (NEAT1) involved in sepsis progression has been reported. [7] However, whether lncRNA nuclear-enriched abundant transcript 1 (NEAT1) regulates asthmatic inflammation and its mechanism still needs to be further investigated. [8] This study aimed to investigate the potential role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in hypertrophic scarring. [9] Additionally, long ncRNA nuclear enriched abundant transcript 1 (NEAT1) is emerging as a vital regulatory molecule in the progression of rheumatoid arthritis (RA). [10] In the current study, we aimed to investigate the expression and biological function of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in ischemia‐induced AKI in patients' sample and in vitro. [11] This study aimed to investigate the predictive value of long noncoding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) for acute ischemic stroke (AIS) risk and to explore the correlation of lncRNA NEAT1 with disease severity, inflammation, recurrence and target microRNAs in patients with AIS. [12] This review summarizes recent literature about the role of the lncRNA nuclear enriched abundant transcript 1 (NEAT1) in non-cancerous diseases with a special focus on viral infections and neurodegenerative diseases. [13] The long non‑coding RNA nuclear enriched abundant transcript 1 (NEAT1) has important roles in the regulation of multiple cell functions, such as proliferation, apoptosis and migration. [14] LncRNA nuclear enriched abundant transcript 1 (NEAT1) was the most significantly downregulated lncRNA in endometrial cancer cells treated with progesterone. [15] It was indicated that lncRNA nuclear enriched abundant transcript 1 (NEAT1) is involved in PD. [16] In this work, we studied the role of the lncRNA nuclear enriched abundant transcript 1 (NEAT1) in the pathogenesis of ACLF. [17] The RNA crosstalk among lncRNA nuclear enriched abundant transcript 1 (NEAT1), miR‐125, and MCEMP1 was validated. [18] Increasing evidence shows that the long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1) plays important roles in tumor progression. [19] We aimed to investigate the roles of the lncRNA nuclear enriched abundant transcript 1 (NEAT1), miR-29b, and autophagy related protein 9a (Atg9a), and their relationships with each other during IGFBPrP1-induced HSC autophagy and activation. [20] In this study, we designed experiments to reveal the role of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in the OGD/R injury of microglial cells. [21] Therefore, currently, we focused on the biological and clinical significance of lncRNA nuclear enriched abundant transcript 1 (NEAT1) and hsa‐mir‐98‐5p in NSCLC. [22] We investigated the role of lncRNA nuclear enriched abundant transcript 1_2 (NEAT1_2) in radioresistance of HCC and its molecular mechanism in this study. [23] LncRNA nuclear enriched abundant transcript 1 (NEAT1) was increased in the cerebral cortex surrounding the injury site of mice after traumatic brain injury, and it promoted the functional recovery in mice. [24] LncRNA nuclear enriched abundant transcript 1 (NEAT1) is a novel lncRNA and has been reported to promote multiple cancer progression. [25] We aimed to investigate the correlation of long noncoding RNA nuclear enriched abundant transcript 1 (lnc-NEAT1), microRNA-124 (miR-124) and lnc-NEAT1/miR-124 axis with disease risk, severity, inflammatory cytokines, and survival of sepsis. [26] LncRNA Nuclear enriched abundant transcript 1 (NEAT1) was involved in multiple tumor formation and biological behaviors of endothelial cells. [27] In this study, we are committed to uncover the potential function of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in the development of laryngocarcinoma. [28] LncRNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to exert a key role in the progression of several diseases including diabetes. [29]현재 연구에서 우리는 ARDS에서 lncRNA 핵이 풍부한 풍부한 전사체 1(NEAT1)의 역할과 기본 메커니즘을 탐구했습니다. [1] 여기, 우리는 지방 형성과 골 형성 사이의 후성 유전 적 조절의 차이점을 프로파일 링하고 노화 된 BMSC의 핵심 뼈 지방 스위치로 슈퍼 인핸서 관련 lncRNA 핵이 풍부한 풍부한 전사체 1(NEAT1)을 확인했습니다. [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] 현재 연구에서 우리는 환자의 샘플 및 시험관 내 허혈 유발 AKI에서 lncRNA 핵 농축 풍부 전사체 1(NEAT1)의 발현 및 생물학적 기능을 조사하는 것을 목표로 하였다. [11] 이 연구는 급성 허혈성 뇌졸중(AIS) 위험에 대한 긴 비암호화 RNA 핵이 풍부한 풍부한 전사체 1(lncRNA NEAT1)의 예측 가치를 조사하고 lncRNA NEAT1과 질병 중증도, 염증, 재발 및 AIS. [12] nan [13] nan [14] nan [15] nan [16] nan [17] nan [18] nan [19] nan [20] nan [21] nan [22] nan [23] nan [24] nan [25] nan [26] nan [27] nan [28] nan [29]
paraspeckle assembly transcript paraspeckle 어셈블리 성적표
LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) was upregulated in response to IR and enhanced GSDME expression by negatively regulating miR-448 expression. [1] Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been identified as an oncogenic gene in multiple human tumors entitles, and dysregulation of NEAT1 was tightly linked to carcinogenesis and cancer progression. [2] This study was dedicated to investigating the regulatory effects of the lncRNA nuclear paraspeckle assembly transcript 1 (Neat1) on liver fibrosis and HSC activation. [3] LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) was also identified as an upstream regulatory factor of hsa-miR-372-3p. [4] Although long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) was reported to be associated with acute lung injury (ALI), its specific mechanism has not been well studied. [5] However, the biological roles of lncRNA Nuclear Paraspeckle Assembly Transcript 1 (NEAT1) in AR are still unclear. [6] The levels of miRNA-101 and lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) were detected by real-time PCR. [7] However, the role of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in colon cancer remains to be further investigated. [8] The lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) contributes to cancer growth through its effects on cell proliferation, migration, invasion and drug resistance. [9] Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) promotes oncogenesis in various tumors. [10] The present study investigated the role of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in CRC. [11] Purpose Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been deemed an oncogene in many human cancers. [12] Previous studies revealed that the long non‑coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) exhibits abnormal expression in numerous cancer types, including breast cancer (BC); however, the regulatory mechanism of NEAT1 in BC remains unclear. [13] LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been recognized as an oncogene to promote tumor progression of many cancers. [14] Accumulating evidence suggested that lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) expression is dysregulated in many human cancers and thus is a useful prognostic marker for cancer patients. [15] In this study, we aim to investigate the effect of long noncoding RNA nuclear paraspeckle assembly transcript 1 (LncRNA NEAT1) on cell viability, sensitivity to 5‐FU, and autophagy of CRC cell lines. [16] Studies have shown that long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) is closely related to the progression of multiple cancers. [17] Herein, we investigated the functional significance of the oncogenic lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in MM. [18] In this study, we found that the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) is significantly increased in both cervical cancer tissues and cell lines. [19] Background Emerging evidence has revealed that long noncoding RNA nuclear paraspeckle assembly transcript 1 (lncRNA NEAT1) is implicated in the development of various cancers. [20] Increasing evidence has suggested that long non‑coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has critical roles in multiple biological processes; however, few studies have reported on its function in heart disease. [21]LncRNA 핵 paraspeckle 어셈블리 전사체 1(NEAT1)은 IR에 대한 반응으로 상향 조절되었고 miR-448 발현을 부정적으로 조절함으로써 GSDME 발현이 향상되었습니다. [1] 긴 비암호화 RNA 핵 파라스페클 어셈블리 전사체 1(NEAT1)은 여러 인간 종양 자격에서 발암성 유전자로 확인되었으며 NEAT1의 조절 장애는 발암 및 암 진행과 밀접하게 연관되어 있습니다. [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] 목적 긴 비암호화 RNA 핵 파라스페클 어셈블리 전사체 1(NEAT1)은 많은 인간 암에서 종양유전자로 간주되었습니다. [12] 이전 연구에 따르면 긴 비암호화 RNA 핵 파라스페클 어셈블리 전사체 1(NEAT1)은 유방암(BC)을 포함한 다양한 암 유형에서 비정상적인 발현을 나타냅니다. 그러나 BC에서 NEAT1의 조절 메커니즘은 아직 명확하지 않습니다. [13] nan [14] nan [15] nan [16] nan [17] nan [18] nan [19] nan [20] nan [21]
long non coding 긴 비 코딩
Accumulating evidences indicate that long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) promotes the progression of glioma. [1] Long non-coding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) drives the malignant phenotypes of EC cells. [2] Background It is reported that long non-coding RNA nuclear paraspeckle assembly transcript 1 (LncRNA NEAT1) is involved in the occurrence and development of various cancers. [3] Previous studies have revealed that long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) exerted critical roles in cancers. [4] Supplemental Digital Content is available in the text The present study aimed to investigate the correlation of long non-coding RNA nuclear-enriched abundant transcript 1 (lncRNA NEAT1) with microRNA (miR)-21, miR-124, and miR-125a, and their associations with disease risk, severity, and inflammatory cytokines of allergic rhinitis (AR). [5] Many long non-coding RNAs (lncRNAs) have been found to play crucial roles in sepsis-induced acute kidney injury (AKI), including lncRNA nuclear-enriched abundant transcript 1 (NEAT1). [6] Previous studies have shown that the long non-coding (lnc)RNA nuclear-enriched abundant transcript 1(NEAT1) participates in various inflammatory conditions and plays an important regulatory role. [7] Objective: Studies have abstracted the partial mechanism of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) in lung cancer, but its reciprocal with microRNA-107/Forkhead box k1 (miR-107/FOXK1) is not disclosed clearly. [8] BACKGROUND Many long non-coding RNAs (lncRNAs) have been suggested to play critical roles in acute lung injury (ALI) pathogenesis, including lncRNA nuclear enriched abundant transcript 1 (NEAT1). [9] Long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported to be associated with T helper 2 (Th2) cell activation. [10] Objective We aimed to investigate the effect of long non-coding RNA nuclear-enriched abundant transcript 1 (lnc-NEAT1) on regulating hepatocyte proliferation, apoptosis, and inflammation during hepatic ischemia/reperfusion (I/R) injury. [11] The purpose of the present study was to investigate the roles of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) and microRNA-455-3p (miR-455-3p) were investigated in pulmonary fibrosis. [12] Background and aim Long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) is abnormally expressed in various human malignancies, including hepatocellular carcinoma (HCC). [13] The present study investigated the expression and clinical significance of the lncRNA nuclear factor-κB interacting long non-coding RNA (NKILA) in CRC. [14] BackgroundThis study aimed to investigate the effect of long non-coding RNA nuclear enriched abundant transcript 1 (lnc-NEAT1) on cell proliferation and apoptosis in myocardial ischemia/reperfusion (I/R) injury cells, and explore its target miRNAs. [15] Furthermore, we identified long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) as a potential hallmark which was down-regulated in ERα silencing HepG2 cells by RNA-Seq. [16] Comprehensive microarray-based analysis demonstrated that nuclear expression of intracellular domain of LRP1B significantly increased the expression of long non-coding RNA nuclear paraspeckle assembly transcript1(NEAT1) , which facilitates breast cancer invasion with poor survival. [17] BACKGROUND Long non-coding RNA Nuclear Paraspeckle Assembly Transcript 1 (NEAT1) is a novel lncRNA localized specifically to nuclear paraspeckles. [18] The long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1), localised in nuclear paraspeckles, has been shown to enhance chemoresistance in several cancer types. [19]축적된 증거는 긴 비암호화 RNA 핵 파라스페클 어셈블리 전사체 1(NEAT1)이 신경아교종의 진행을 촉진한다는 것을 나타냅니다. [1] 긴 비암호화 RNA 핵이 풍부한 풍부한 전사체 1(lncRNA NEAT1)은 EC 세포의 악성 표현형을 구동합니다. [2] 배경 긴 비암호화 RNA 핵 파라스페클 어셈블리 전사체 1(LncRNA NEAT1)은 다양한 암의 발생 및 발달에 관여하는 것으로 보고되고 있다. [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12] 배경 및 목표 Long non-coding RNA 핵농축 풍부 전사체 1(NEAT1)은 간세포 암종(HCC)을 비롯한 다양한 인간 악성 종양에서 비정상적으로 발현됩니다. [13] 본 연구는 CRC에서 긴 비암호화 RNA(NKILA)와 상호작용하는 lncRNA 핵 인자-κB의 발현 및 임상적 중요성을 조사하였다. [14] 배경 이 연구는 심근 허혈/재관류(I/R) 손상 세포에서 세포 증식 및 세포 사멸에 대한 긴 비암호화 RNA 핵 농축 풍부 전사체 1(lnc-NEAT1)의 영향을 조사하고 표적 miRNA를 탐색하는 것을 목표로 했습니다. [15] nan [16] nan [17] nan [18] nan [19]
abundant transcript 1
This study aims to define the role of long noncoding RNA nuclear‐enriched abundant transcript 1 (lncRNA NEAT1) and its downstream molecule in Th17 cell differentiation. [1] The long noncoding RNA nuclear‐enriched abundant transcript 1 (NEAT1) is reportedly involved in the initiation and progression of cancers of several types. [2] LncRNA nuclear‐enriched abundant transcript 1 (NEAT1) participates in the development and progression of multiple malignancies. [3] This study aimed to explore the association of long non‐coding RNA nuclear‐enriched abundant transcript 1 (lncRNA NEAT1) with exacerbation risk, lung function, and inflammatory cytokines in asthma. [4] The aim of this work was to explore the functional role of lncRNA nuclear‐enriched abundant transcript 1 (NEAT1) in OA. [5]이 연구는 Th17 세포 분화에서 긴 비암호화 RNA 핵이 풍부한 풍부한 전사체 1(lncRNA NEAT1)과 그 다운스트림 분자의 역할을 정의하는 것을 목표로 합니다. [1] 긴 비암호화 RNA 핵이 풍부한 풍부한 전사체 1(NEAT1)은 여러 유형의 암의 시작 및 진행에 관여하는 것으로 보고됩니다. [2] nan [3] nan [4] nan [5]
assembly transcript 1 어셈블리 성적표 1
This study intended to investigate the role of lncRNA nuclear enriched assembly transcript 1 (NEAT1) in MPP+-induced PD model in dopaminergic neuronblastoma SK-N-SH cells, as well as its mechanism through sponging miRNA (miR)-1277-5p. [1]이 연구는 도파민성 신경모세포종 SK-N-SH 세포에서 MPP+로 유도된 PD 모델에서 lncRNA 핵 농축 어셈블리 전사체 1(NEAT1)의 역할과 스폰지 miRNA(miR)-1277-5p를 통한 메커니즘을 조사하기 위한 것입니다. [1]
Coding Rna Nuclear 코딩 Rna 핵
Accumulating evidences indicate that long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) promotes the progression of glioma. [1] Long non-coding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) drives the malignant phenotypes of EC cells. [2] Background It is reported that long non-coding RNA nuclear paraspeckle assembly transcript 1 (LncRNA NEAT1) is involved in the occurrence and development of various cancers. [3] Previous studies have revealed that long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) exerted critical roles in cancers. [4] Supplemental Digital Content is available in the text The present study aimed to investigate the correlation of long non-coding RNA nuclear-enriched abundant transcript 1 (lncRNA NEAT1) with microRNA (miR)-21, miR-124, and miR-125a, and their associations with disease risk, severity, and inflammatory cytokines of allergic rhinitis (AR). [5] Objective: Studies have abstracted the partial mechanism of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) in lung cancer, but its reciprocal with microRNA-107/Forkhead box k1 (miR-107/FOXK1) is not disclosed clearly. [6] Long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported to be associated with T helper 2 (Th2) cell activation. [7] Objective We aimed to investigate the effect of long non-coding RNA nuclear-enriched abundant transcript 1 (lnc-NEAT1) on regulating hepatocyte proliferation, apoptosis, and inflammation during hepatic ischemia/reperfusion (I/R) injury. [8] The purpose of the present study was to investigate the roles of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) and microRNA-455-3p (miR-455-3p) were investigated in pulmonary fibrosis. [9] Background and aim Long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) is abnormally expressed in various human malignancies, including hepatocellular carcinoma (HCC). [10] BackgroundThis study aimed to investigate the effect of long non-coding RNA nuclear enriched abundant transcript 1 (lnc-NEAT1) on cell proliferation and apoptosis in myocardial ischemia/reperfusion (I/R) injury cells, and explore its target miRNAs. [11] Previous studies revealed that the long non‑coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) exhibits abnormal expression in numerous cancer types, including breast cancer (BC); however, the regulatory mechanism of NEAT1 in BC remains unclear. [12] Furthermore, we identified long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) as a potential hallmark which was down-regulated in ERα silencing HepG2 cells by RNA-Seq. [13] Comprehensive microarray-based analysis demonstrated that nuclear expression of intracellular domain of LRP1B significantly increased the expression of long non-coding RNA nuclear paraspeckle assembly transcript1(NEAT1) , which facilitates breast cancer invasion with poor survival. [14] BACKGROUND Long non-coding RNA Nuclear Paraspeckle Assembly Transcript 1 (NEAT1) is a novel lncRNA localized specifically to nuclear paraspeckles. [15] The long non‑coding RNA nuclear enriched abundant transcript 1 (NEAT1) has important roles in the regulation of multiple cell functions, such as proliferation, apoptosis and migration. [16] This study aimed to explore the association of long non‐coding RNA nuclear‐enriched abundant transcript 1 (lncRNA NEAT1) with exacerbation risk, lung function, and inflammatory cytokines in asthma. [17] Increasing evidence has suggested that long non‑coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has critical roles in multiple biological processes; however, few studies have reported on its function in heart disease. [18] The long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1), localised in nuclear paraspeckles, has been shown to enhance chemoresistance in several cancer types. [19]축적된 증거는 긴 비암호화 RNA 핵 파라스페클 어셈블리 전사체 1(NEAT1)이 신경아교종의 진행을 촉진한다는 것을 나타냅니다. [1] 긴 비암호화 RNA 핵이 풍부한 풍부한 전사체 1(lncRNA NEAT1)은 EC 세포의 악성 표현형을 구동합니다. [2] 배경 긴 비암호화 RNA 핵 파라스페클 어셈블리 전사체 1(LncRNA NEAT1)은 다양한 암의 발생 및 발달에 관여하는 것으로 보고되고 있다. [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] 배경 및 목표 Long non-coding RNA 핵농축 풍부 전사체 1(NEAT1)은 간세포 암종(HCC)을 비롯한 다양한 인간 악성 종양에서 비정상적으로 발현됩니다. [10] 배경 이 연구는 심근 허혈/재관류(I/R) 손상 세포에서 세포 증식 및 세포 사멸에 대한 긴 비암호화 RNA 핵 농축 풍부 전사체 1(lnc-NEAT1)의 영향을 조사하고 표적 miRNA를 탐색하는 것을 목표로 했습니다. [11] 이전 연구에 따르면 긴 비암호화 RNA 핵 파라스페클 어셈블리 전사체 1(NEAT1)은 유방암(BC)을 포함한 다양한 암 유형에서 비정상적인 발현을 나타냅니다. 그러나 BC에서 NEAT1의 조절 메커니즘은 아직 명확하지 않습니다. [12] nan [13] nan [14] nan [15] nan [16] nan [17] nan [18] nan [19]
Noncoding Rna Nuclear 비코딩 Rna 핵
Long noncoding RNA nuclear receptor subfamily 2 group F member 1 antisense RNA 1 (NR2F1-AS1) is dysregulated in HCC. [1] Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been identified as an oncogenic gene in multiple human tumors entitles, and dysregulation of NEAT1 was tightly linked to carcinogenesis and cancer progression. [2] Although long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) was reported to be associated with acute lung injury (ALI), its specific mechanism has not been well studied. [3] This study aims to evaluate the predictive value of serum exosomal long noncoding RNA nuclear-enriched abundant transcript 1 (lncRNA NEAT1) for 90-day mortality of ACHBLF. [4] Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) promotes oncogenesis in various tumors. [5] Apparently, long noncoding RNA nuclear-enriched autosomal transcript 1 (NEAT1) has been identified as a tumor promoter in multiple cancers. [6] This study aims to define the role of long noncoding RNA nuclear‐enriched abundant transcript 1 (lncRNA NEAT1) and its downstream molecule in Th17 cell differentiation. [7] Purpose Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been deemed an oncogene in many human cancers. [8] The long noncoding RNA nuclear‐enriched abundant transcript 1 (NEAT1) is reportedly involved in the initiation and progression of cancers of several types. [9] Currently, long noncoding RNA nuclear RNA host gene 7 (SNHG7) is recognized as a biomarker of multiple cancers. [10] This study aimed to investigate the predictive value of long noncoding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) for acute ischemic stroke (AIS) risk and to explore the correlation of lncRNA NEAT1 with disease severity, inflammation, recurrence and target microRNAs in patients with AIS. [11] In this study, we aim to investigate the effect of long noncoding RNA nuclear paraspeckle assembly transcript 1 (LncRNA NEAT1) on cell viability, sensitivity to 5‐FU, and autophagy of CRC cell lines. [12] Studies have shown that long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) is closely related to the progression of multiple cancers. [13] Increasing evidence shows that the long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1) plays important roles in tumor progression. [14] We aimed to investigate the correlation of long noncoding RNA nuclear enriched abundant transcript 1 (lnc-NEAT1), microRNA-124 (miR-124) and lnc-NEAT1/miR-124 axis with disease risk, severity, inflammatory cytokines, and survival of sepsis. [15] Background Emerging evidence has revealed that long noncoding RNA nuclear paraspeckle assembly transcript 1 (lncRNA NEAT1) is implicated in the development of various cancers. [16]긴 비암호화 RNA 핵 수용체 서브패밀리 2 그룹 F 구성원 1 안티센스 RNA 1(NR2F1-AS1)은 HCC에서 조절되지 않습니다. [1] 긴 비암호화 RNA 핵 파라스페클 어셈블리 전사체 1(NEAT1)은 여러 인간 종양 자격에서 발암성 유전자로 확인되었으며 NEAT1의 조절 장애는 발암 및 암 진행과 밀접하게 연관되어 있습니다. [2] nan [3] nan [4] nan [5] 분명히, 긴 비암호화 RNA 핵이 풍부한 상염색체 전사체 1(NEAT1)은 여러 암에서 종양 프로모터로 확인되었습니다. [6] 이 연구는 Th17 세포 분화에서 긴 비암호화 RNA 핵이 풍부한 풍부한 전사체 1(lncRNA NEAT1)과 그 다운스트림 분자의 역할을 정의하는 것을 목표로 합니다. [7] 목적 긴 비암호화 RNA 핵 파라스페클 어셈블리 전사체 1(NEAT1)은 많은 인간 암에서 종양유전자로 간주되었습니다. [8] 긴 비암호화 RNA 핵이 풍부한 풍부한 전사체 1(NEAT1)은 여러 유형의 암의 시작 및 진행에 관여하는 것으로 보고됩니다. [9] nan [10] 이 연구는 급성 허혈성 뇌졸중(AIS) 위험에 대한 긴 비암호화 RNA 핵이 풍부한 풍부한 전사체 1(lncRNA NEAT1)의 예측 가치를 조사하고 lncRNA NEAT1과 질병 중증도, 염증, 재발 및 AIS. [11] nan [12] nan [13] nan [14] nan [15] nan [16]
Viral Rna Nuclear
However, other cellular factors that are involved in the CRM1-dependent viral RNA nuclear export remain largely unknown. [1] However, other cellular factors involved in the CRM1-dependent viral RNA nuclear export remain largely unknown. [2]그러나 CRM1-의존성 바이러스 RNA 핵 수출에 관여하는 다른 세포 요인은 크게 알려지지 않았습니다. [1] 그러나 CRM1 의존성 바이러스 RNA 핵 수출과 관련된 다른 세포 요인은 크게 알려지지 않았습니다. [2]
Circular Rna Nuclear 원형 Rna 핵
In total, this approach can be broadly used to characterize circular RNA nuclear export and localization mechanisms, including to identify novel regulatory factors and their breadth of circular RNA targets. [1] The present study aimed to investigate the influence of circular RNA nuclear receptor-interacting protein 1 (circNRIP1) on the chemotherapeutic effect of 5-fluorouracil (5-FU) in colorectal cancer (CRC) and reveal its potential molecular mechanisms. [2]전체적으로, 이 접근 방식은 새로운 규제 요인과 순환 RNA 표적의 폭을 식별하는 것을 포함하여 순환 RNA 핵 수출 및 현지화 메커니즘을 특성화하는 데 광범위하게 사용될 수 있습니다. [1] 현재 연구는 원형 RNA 핵 수용체-상호작용 단백질 1(circNRIP1)이 결장직장암(CRC)에서 5-플루오로우라실(5-FU)의 화학요법 효과에 미치는 영향을 조사하고 잠재적인 분자 메커니즘을 밝히는 것을 목표로 하고 있습니다. [2]
rna nuclear export Rna 원자력 수출
This trafficking has been implicated in facilitating gRNA nuclear export and is thought to be a required mechanism. [1] KSHV SOX, encoded by the open reading frame 37 (ORF37), induces a widespread cytoplasmic mRNA degradation and a block on mRNA nuclear export. [2] We found that hnRNPAB was associated with PB2 mRNA and overexpression of hnRNPAB reduced PB2 mRNA nuclear export and PB2 protein level, but had no influence on PB2 mRNA level. [3] In addition, the regulatory mechanism of MAT2A mRNA nuclear export was investigated by transfection, plasma nucleation separation, and co-immunoprecipitation. [4] We go on to demonstrate that LENG8 binds to mRNAs, associates with components of mRNA processing machinery (the TREX complex) and contributes to mRNA nuclear export to the cytoplasm. [5] DSS1, a component of the TRanscription–EXport-2 (TREX-2) complex involved in transcription and mRNA nuclear export, stabilizes BRCA2 expression. [6] NXT1 heterodimerizes with NXF1 and together they form the principle mRNA nuclear export machinery. [7] Balancing mRNA nuclear export kinetics with its nuclear decay is critical for mRNA homeostasis control. [8] This trafficking has been implicated in facilitating gRNA nuclear export and is thought to be a required mechanism. [9] In this study, we report that hnRNPAB cooperates with nucleoprotein (NP) to restrict viral mRNA nuclear export via inhibiting viral mRNA binding to ALY and NXF1. [10] We show that globally inhibiting mRNA nuclear export by anchoring away mRNA biogenesis or export factors out of the nucleus can recapitulate RMD hyper-activation in the absence of stress. [11] By modulating pre-mRNA splicing, mRNA nuclear export, decay, stability, and translation of oncogenic and tumor suppressive transcripts, RNA m6A modification proteins regulate cancer cell proliferation, survival, migration, invasion, tumor initiation, progression, metastasis, and sensitivity to anticancer therapies. [12] In total, this approach can be broadly used to characterize circular RNA nuclear export and localization mechanisms, including to identify novel regulatory factors and their breadth of circular RNA targets. [13] Pachytene piRNA precursor transcripts bind THOC1 and THOC2, THO complex subunits known to promote transcriptional elongation and mRNA nuclear export. [14] Moreover, a quantitative proteomics approach confirmed PGC-1α-dependent RNA transport and mitochondrial-related functions, identifying also novel mRNA nuclear export targets in age-related telomere maintenance. [15] Conclusions Circ_0004296 overexpression efficiently inhibited ETS1 mRNA nuclear export by promoting EIF4A3 retention in the nucleus, leading to the downregulation of ETS1 expression and suppression of PCa metastasis; thus, circ_0004296 might be a potential biomarker and therapeutic target for patients with PCa. [16] Complete depletion of Nup153 and Nup50 results in an mRNA nuclear export efficiency decrease of approximately four folds. [17] RNA methylations regulate almost all aspects of RNA processing, such as RNA nuclear export, translation, splicing and non-coding RNA processing. [18] SLBP is also involved in regulation of histone mRNA nuclear export, degradation, and translation. [19] Pab1, the major poly (A) binding protein of the yeast Saccharomyces cerevisiae, is involved in many intracellular functions associated with mRNA metabolism, such as mRNA nuclear export, deadenylation, translation initiation and termination. [20] The nuclear retention defect can be mitigated by wild-type but not nuclear export-deficient FMRP, establishing a critical role for FMRP in mediating m6A-dependent mRNA nuclear export during neural differentiation. [21] However, the results also suggest roles for CDK12 in other events, notably mRNA nuclear export, cell differentiation and mitosis. [22] Unexpectedly, NRDE2 mainly localizes in nuclear speckles, where it inhibits MTR4 recruitment and RNA degradation, and thereby ensures efficient mRNA nuclear export. [23] The PRRSV nsp1β protein blocks host mRNA nuclear export, which has been shown to be one of the viral mechanisms for inhibition of antiviral protein production. [24] By characterizing expression of both pre-miRNAs and mature miRNAs under various conditions, this study revealed striking differences in miRNA biogenesis between lytic and latent infection and uncovered a regulatory mechanism that blocks pre-miRNA nuclear export and is dependent on viral protein ICP27 and viral DNA synthesis. [25] Together, our findings demonstrate a unique and pivotal role of Tpr in regulating gene expression through GANP- and/or NXF1-dependent mRNA nuclear export. [26] However, other cellular factors that are involved in the CRM1-dependent viral RNA nuclear export remain largely unknown. [27] In this review, we firstly evaluate the necessity of single-molecule live-cell microscopy in the study of mRNA nuclear export. [28] Taken together, our findings revealed that eIF4A3 is a key mediator of AIV polymerase activity, mRNA splicing, and spliced mRNA nuclear export. [29] Mammalian cytoplasmic poly(A) binding protein (PABPC) protects mRNA transcripts from deadenylation and 3’ end degradation, facilitates mRNA nuclear export and mRNA translation. [30] NUP214 is a component of the nuclear pore complex (NPC) with a key role in protein and mRNA nuclear export. [31] In search of alternative pathways, we tested the mRNA export complex Mex67-Mtr2, for a role in tRNA nuclear export, as described previously in yeast. [32] In this point-of-view article, we will discuss our recently identified circRNA nuclear export pathway and address important open questions in the field. [33] However, other cellular factors involved in the CRM1-dependent viral RNA nuclear export remain largely unknown. [34] Although the components of this machinery have been identified and considerable functional insight has been achieved, a number of questions remain outstanding about mRNA nuclear export and how it is integrated into the nuclear phase of the gene expression pathway. [35] Here we investigate the role of the major nuclear pore basket protein, TPR, in regulating mRNA and lncRNA nuclear export in human cells. [36] Interestingly, given its key role as a regulator of RNA splicing, we found that TARDBP has an inhibitory role on pregenomic RNA splicing, which might help the virus to export its non-canonical RNAs from the nucleus without being subjected to unwanted splicing, even though mRNA nuclear export is normally closely tied to RNA splicing. [37] These structures have facilitated the engineering of mutants that have been used to define the contributions made by the TREX-2 complex to locating high-expressed genes to nuclear pores and the contributions made to mRNA nuclear export. [38] KPT-330 generally mitigated mRNA expression and protein synthesis rather than mRNA nuclear export or protein stability of Mcl-1. [39]이 인신매매는 gRNA 핵 수출을 촉진하는 것과 관련이 있으며 필요한 메커니즘으로 생각됩니다. [1] 오픈 리딩 프레임 37(ORF37)에 의해 암호화된 KSHV SOX는 광범위한 세포질 mRNA 분해 및 mRNA 핵 내보내기 차단을 유도합니다. [2] 우리는 hnRNPAB이 PB2 mRNA와 관련이 있고 hnRNPAB의 과발현이 PB2 mRNA 핵 수출 및 PB2 단백질 수준을 감소시켰지만 PB2 mRNA 수준에는 영향을 미치지 않는다는 것을 발견했습니다. [3] 또한, MAT2A mRNA 핵 수출의 조절 메커니즘은 형질감염, 혈장 핵형성 분리 및 공동 면역 침전에 의해 조사되었다. [4] 우리는 LENG8이 mRNA에 결합하고 mRNA 처리 기계(TREX 복합체)의 구성요소와 연관되며 세포질로의 mRNA 핵 수출에 기여한다는 것을 계속 입증합니다. [5] 전사 및 mRNA 핵 내보내기에 관여하는 TREX-2(TRanscription-EXport-2) 복합체의 구성요소인 DSS1은 BRCA2 발현을 안정화합니다. [6] NXT1은 NXF1과 이형이량체화되어 함께 주요 mRNA 핵 수출 기계를 형성합니다. [7] mRNA 핵 수출 동역학과 핵 붕괴의 균형을 맞추는 것은 mRNA 항상성 제어에 중요합니다. [8] 이 인신매매는 gRNA 핵 수출을 촉진하는 것과 관련이 있으며 필요한 메커니즘으로 생각됩니다. [9] 이 연구에서 우리는 hnRNPAB이 핵단백질(NP)과 협력하여 ALY 및 NXF1에 대한 바이러스 mRNA 결합을 억제함으로써 바이러스 mRNA 핵 수출을 제한한다고 보고합니다. [10] 우리는 mRNA 생물 생성을 고정함으로써 mRNA 핵 수출을 전 세계적으로 억제하거나 핵 밖으로 인자를 내보내는 것이 스트레스가 없을 때 RMD 과활성화를 요약할 수 있음을 보여줍니다. [11] pre-mRNA 스플라이싱, mRNA 핵 내보내기, 붕괴, 안정성 및 발암성 및 종양 억제 전사체의 번역을 조절함으로써 RNA m6A 변형 단백질은 암세포 증식, 생존, 이동, 침습, 종양 개시, 진행, 전이 및 항암 감수성을 조절합니다 치료법. [12] 전체적으로, 이 접근 방식은 새로운 규제 요인과 순환 RNA 표적의 폭을 식별하는 것을 포함하여 순환 RNA 핵 수출 및 현지화 메커니즘을 특성화하는 데 광범위하게 사용될 수 있습니다. [13] Pachytene piRNA 전구체 전사체는 전사 신장 및 mRNA 핵 수출을 촉진하는 것으로 알려진 THO 복합 소단위인 THOC1 및 THOC2에 결합합니다. [14] 또한, 정량적 단백질체학 접근법은 PGC-1α 의존성 RNA 수송 및 미토콘드리아 관련 기능을 확인하여 연령 관련 텔로미어 유지에서 새로운 mRNA 핵 수출 표적을 식별했습니다. [15] 결론 Circ_0004296 과발현은 핵에서 EIF4A3 보유를 촉진하여 ETS1 mRNA 핵 내보내기를 효율적으로 억제하여 ETS1 발현의 하향 조절 및 PCa 전이의 억제를 유도했습니다. 따라서 circ_0004296은 PCa 환자의 잠재적 바이오마커 및 치료 표적이 될 수 있습니다. [16] Nup153 및 Nup50이 완전히 고갈되면 mRNA 핵 수출 효율이 약 4배 감소합니다. [17] RNA 메틸화는 RNA 핵 수출, 번역, 스플라이싱 및 비코딩 RNA 처리와 같은 RNA 처리의 거의 모든 측면을 조절합니다. [18] SLBP는 또한 히스톤 mRNA 핵 수출, 분해 및 번역의 조절에 관여합니다. [19] 효모 Saccharomyces cerevisiae의 주요 폴리(A) 결합 단백질인 Pab1은 mRNA 핵 수출, 데데닐화, 번역 개시 및 종결과 같은 mRNA 대사와 관련된 많은 세포내 기능에 관여한다. [20] 핵 보유 결함은 야생형에 의해 완화될 수 있지만 핵 수출이 부족한 FMRP는 완화되지 않으며, 신경 분화 동안 m6A 의존성 mRNA 핵 수출을 매개하는 FMRP에 대한 중요한 역할을 설정합니다. [21] nan [22] nan [23] nan [24] nan [25] nan [26] 그러나 CRM1-의존성 바이러스 RNA 핵 수출에 관여하는 다른 세포 요인은 크게 알려지지 않았습니다. [27] nan [28] nan [29] nan [30] nan [31] nan [32] nan [33] 그러나 CRM1 의존성 바이러스 RNA 핵 수출과 관련된 다른 세포 요인은 크게 알려지지 않았습니다. [34] nan [35] nan [36] nan [37] nan [38] nan [39]
rna nuclear enriched Rna 핵 농축
Long non-coding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) drives the malignant phenotypes of EC cells. [1] In the present study, we explored the roles and underlying mechanism of the lncRNA Nuclear enriched abundant transcript 1 (NEAT1) in ARDS. [2] Objective: Studies have abstracted the partial mechanism of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) in lung cancer, but its reciprocal with microRNA-107/Forkhead box k1 (miR-107/FOXK1) is not disclosed clearly. [3] BACKGROUND Many long non-coding RNAs (lncRNAs) have been suggested to play critical roles in acute lung injury (ALI) pathogenesis, including lncRNA nuclear enriched abundant transcript 1 (NEAT1). [4] However, the mechanism underlying the influence of the lncRNA nuclear enriched abundant transcripts 1 (NEAT1) on CSF is still unknown. [5] This study intended to investigate the role of lncRNA nuclear enriched assembly transcript 1 (NEAT1) in MPP+-induced PD model in dopaminergic neuronblastoma SK-N-SH cells, as well as its mechanism through sponging miRNA (miR)-1277-5p. [6] This study aimed to investigate the potential role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in hypertrophic scarring. [7] Additionally, long ncRNA nuclear enriched abundant transcript 1 (NEAT1) is emerging as a vital regulatory molecule in the progression of rheumatoid arthritis (RA). [8] The purpose of the present study was to investigate the roles of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) and microRNA-455-3p (miR-455-3p) were investigated in pulmonary fibrosis. [9] BackgroundThis study aimed to investigate the effect of long non-coding RNA nuclear enriched abundant transcript 1 (lnc-NEAT1) on cell proliferation and apoptosis in myocardial ischemia/reperfusion (I/R) injury cells, and explore its target miRNAs. [10] In the current study, we aimed to investigate the expression and biological function of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in ischemia‐induced AKI in patients' sample and in vitro. [11] Furthermore, we identified long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) as a potential hallmark which was down-regulated in ERα silencing HepG2 cells by RNA-Seq. [12] This study aimed to investigate the predictive value of long noncoding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) for acute ischemic stroke (AIS) risk and to explore the correlation of lncRNA NEAT1 with disease severity, inflammation, recurrence and target microRNAs in patients with AIS. [13] This review summarizes recent literature about the role of the lncRNA nuclear enriched abundant transcript 1 (NEAT1) in non-cancerous diseases with a special focus on viral infections and neurodegenerative diseases. [14] The long non‑coding RNA nuclear enriched abundant transcript 1 (NEAT1) has important roles in the regulation of multiple cell functions, such as proliferation, apoptosis and migration. [15] LncRNA nuclear enriched abundant transcript 1 (NEAT1) was the most significantly downregulated lncRNA in endometrial cancer cells treated with progesterone. [16] It was indicated that lncRNA nuclear enriched abundant transcript 1 (NEAT1) is involved in PD. [17] In this work, we studied the role of the lncRNA nuclear enriched abundant transcript 1 (NEAT1) in the pathogenesis of ACLF. [18] The RNA crosstalk among lncRNA nuclear enriched abundant transcript 1 (NEAT1), miR‐125, and MCEMP1 was validated. [19] Increasing evidence shows that the long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1) plays important roles in tumor progression. [20] We aimed to investigate the roles of the lncRNA nuclear enriched abundant transcript 1 (NEAT1), miR-29b, and autophagy related protein 9a (Atg9a), and their relationships with each other during IGFBPrP1-induced HSC autophagy and activation. [21] In this study, we designed experiments to reveal the role of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in the OGD/R injury of microglial cells. [22] Therefore, currently, we focused on the biological and clinical significance of lncRNA nuclear enriched abundant transcript 1 (NEAT1) and hsa‐mir‐98‐5p in NSCLC. [23] We investigated the role of lncRNA nuclear enriched abundant transcript 1_2 (NEAT1_2) in radioresistance of HCC and its molecular mechanism in this study. [24] LncRNA nuclear enriched abundant transcript 1 (NEAT1) was increased in the cerebral cortex surrounding the injury site of mice after traumatic brain injury, and it promoted the functional recovery in mice. [25] LncRNA nuclear enriched abundant transcript 1 (NEAT1) is a novel lncRNA and has been reported to promote multiple cancer progression. [26] We aimed to investigate the correlation of long noncoding RNA nuclear enriched abundant transcript 1 (lnc-NEAT1), microRNA-124 (miR-124) and lnc-NEAT1/miR-124 axis with disease risk, severity, inflammatory cytokines, and survival of sepsis. [27] LncRNA Nuclear enriched abundant transcript 1 (NEAT1) was involved in multiple tumor formation and biological behaviors of endothelial cells. [28] In this study, we are committed to uncover the potential function of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in the development of laryngocarcinoma. [29] LncRNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to exert a key role in the progression of several diseases including diabetes. [30]긴 비암호화 RNA 핵이 풍부한 풍부한 전사체 1(lncRNA NEAT1)은 EC 세포의 악성 표현형을 구동합니다. [1] 현재 연구에서 우리는 ARDS에서 lncRNA 핵이 풍부한 풍부한 전사체 1(NEAT1)의 역할과 기본 메커니즘을 탐구했습니다. [2] nan [3] nan [4] nan [5] 이 연구는 도파민성 신경모세포종 SK-N-SH 세포에서 MPP+로 유도된 PD 모델에서 lncRNA 핵 농축 어셈블리 전사체 1(NEAT1)의 역할과 스폰지 miRNA(miR)-1277-5p를 통한 메커니즘을 조사하기 위한 것입니다. [6] nan [7] nan [8] nan [9] 배경 이 연구는 심근 허혈/재관류(I/R) 손상 세포에서 세포 증식 및 세포 사멸에 대한 긴 비암호화 RNA 핵 농축 풍부 전사체 1(lnc-NEAT1)의 영향을 조사하고 표적 miRNA를 탐색하는 것을 목표로 했습니다. [10] 현재 연구에서 우리는 환자의 샘플 및 시험관 내 허혈 유발 AKI에서 lncRNA 핵 농축 풍부 전사체 1(NEAT1)의 발현 및 생물학적 기능을 조사하는 것을 목표로 하였다. [11] nan [12] 이 연구는 급성 허혈성 뇌졸중(AIS) 위험에 대한 긴 비암호화 RNA 핵이 풍부한 풍부한 전사체 1(lncRNA NEAT1)의 예측 가치를 조사하고 lncRNA NEAT1과 질병 중증도, 염증, 재발 및 AIS. [13] nan [14] nan [15] nan [16] nan [17] nan [18] nan [19] nan [20] nan [21] nan [22] nan [23] nan [24] nan [25] nan [26] nan [27] nan [28] nan [29] nan [30]