Translocation Gene(전좌 유전자)란 무엇입니까?
Translocation Gene 전좌 유전자 - Furthermore, the identified pronounced deleterious effects of PAX7-FOXO1 provide an explanation for the low frequency of the translocation generating this factor in patients with rhabdomyosarcoma. [1] Furthermore, in mnb1 mutants, the transcription level of the Fe-uptake and translocation genes, FIT , IRT1 , FRO2 , Z IF , FRD3 , NAS4 , PYE and MYB72 , were considerably elevated during Fe-deficiency stress, resulting in higher Fe accumulation. [2] Structure analysis revealed integration of the translocated animals and evidence of a unique post-translocation genetic cluster. [3] The t(8;21) translocation generates the aberrant transcription factor RUNX1-ETO whose expression can be detected in utero but is insufficient to cause overt disease. [4] The t(8;21)(q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoietic master regulator RUNX1. [5] His cytogenetic analysis showed the t(9;22) translocation generating the Philadelphia chromosome (Ph), with a multiplex RT-PCR detecting an atypical fragment. [6] Central features of the T3SS are a highly conserved set of secretion and translocation genes and contact dependence wherein host-pathogen interactions trigger effector protein delivery and serve as an inducing signal for T3SS gene expression. [7]또한, 확인된 PAX7-FOXO1의 현저한 유해 효과는 횡문근육종 환자에서 이 인자를 생성하는 전위의 빈도가 낮은 이유를 설명합니다. [1] 또한, mnb1 돌연변이에서 Fe-흡수 및 전위 유전자인 FIT, IRT1, FRO2, Z IF, FRD3, NAS4, PYE 및 MYB72의 전사 수준은 Fe-결핍 스트레스 동안 상당히 증가하여 Fe 축적이 더 높아졌습니다. [2] 구조 분석은 전위된 동물의 통합과 독특한 전위 후 유전자 클러스터의 증거를 보여주었습니다. [3] t(8;21) 전위는 자궁 내에서 발현이 감지될 수 있지만 명백한 질병을 일으키기에는 불충분한 비정상적인 전사 인자 RUNX1-ETO를 생성합니다. [4] t(8;21)(q22;q22) 전위는 조혈 마스터 레귤레이터 RUNX1을 방해하는 RUNX1-ETO 융합 단백질을 생성합니다. [5] 그의 세포유전학적 분석은 비정형 단편을 검출하는 멀티플렉스 RT-PCR과 함께 필라델피아 염색체(Ph)를 생성하는 t(9;22) 전위를 보여주었습니다. [6] T3SS의 중심 특징은 고도로 보존된 분비 및 전위 유전자 세트와 숙주-병원체 상호작용이 이펙터 단백질 전달을 유발하고 T3SS 유전자 발현을 위한 유도 신호로 작용하는 접촉 의존성입니다. [7]
dual luciferase reporter 이중 루시퍼라제 리포터
Dual luciferase reporter assay further showed that miR-934 directly bound to B-cell translocation gene 2 (BTG2). [1] The relation between B-cell translocation gene 1 (BTG1) and miR-330-3p was predicted by TargetScan and confirmed by dual-luciferase reporter assay. [2] Mechanically, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) identified that HOTAIRM1 and B-cell translocation gene 3 (BTG3) were target genes of miR-17-5p. [3] A dual-luciferase reporter assay was performed to validate B-cell translocation gene 3 (BTG3) as a target of miR-20b-5p. [4]이중 루시퍼라제 리포터 분석은 miR-934가 B-세포 전위 유전자 2(BTG2)에 직접 결합함을 추가로 보여주었습니다. [1] B-세포 전위 유전자 1(BTG1)과 miR-330-3p 사이의 관계는 TargetScan에 의해 예측되었고 이중 루시퍼라제 리포터 분석에 의해 확인되었습니다. [2] 기계적으로, 이중 루시퍼라제 리포터 분석 및 RNA 면역 침전(RIP)은 HOTAIRM1 및 B-세포 전위 유전자 3(BTG3)이 miR-17-5p의 표적 유전자임을 확인했습니다. [3] nan [4]
Cell Translocation Gene 세포 전위 유전자
B‐cell translocation gene 2 (BTG2) was identified to be a direct target of miR‐365, while the focal adhesion kinase (F/ATP)‐dependent tyrosine kinase (AKT) pathway was activated by miR‐365. [1] Knockout of B-cell translocation gene-4 (Btg4), an adaptor protein of the CCR4-NOT complex, results in mRNA decay defects following fertilization. [2] This study aimed to investigate the role of cleavage and polyadenylation factor-6 (CPSF6) and B-cell translocation gene 2 (BTG2) in regulating the glycolysis and apoptosis in HCC cells. [3] B-cell translocation gene 2 (BTG2) and yin yang 1 (YY1) are key regulators of diverse metabolic processes. [4] B-cell translocation gene 1 (BTG1) mRNA was identified as the novel target of miR-301a-3p. [5] This research aims to probe the protective effects of exosomal miR-150-5p from BMSCs on cerebral I/R injury via regulating B-cell translocation gene 2 (BTG2). [6] Objective: In this study, we wanted to investigate the plasma exosome-derived B-cell translocation gene 1 (BTG-1) level as a predictive marker for the prognosis in patients with Non-small cell lung cancer (NSCLC). [7] METHODS The expression levels of miR-183-5p and B-cell translocation gene 1 (Btg1) were determined by quantitative real-time PCR and histological analysis in livers of obese mice and cell models induced with palmitic acid (PA), respectively. [8] The current paper gives prominence to the role of miR-322-5p in MI by regulating B-cell translocation gene 2 (BTG2). [9] Dual luciferase reporter assay further showed that miR-934 directly bound to B-cell translocation gene 2 (BTG2). [10] Hence, this study intends to unearth the mechanism of AD, mainly focusing on miR-16-5p/B-cell translocation gene 2 (BTG2) axis. [11] A luciferase assay revealed that B-cell translocation gene 2 (BTG2) was a target gene of miR-15a and negatively correlated with miR-15a expression. [12] An ovalbumin-induced mouse asthma model was established, followed by injection of short hairpin RNA (sh)-EZH2, overexpression-B-cell translocation gene 2 (oe-BTG2), microRNA (miR)-34b agomir as well as their corresponding controls. [13] This review covers the following topics: tumor-promoting activity of the Tipα family members HP-MP1 and Tipα, the mechanism underlying this activity of Tipα via binding to the cell-surface receptor, nucleolin, the crystal structure of rdel-Tipα and N-terminal truncated rTipα, inhibition of Tipα-associated gastric carcinogenesis by tumor suppressor B-cell translocation gene 2 (BTG2/TIS21), and new strategies to prevent and treat gastric cancer. [14] In this study, we used a mouse model of bilateral common carotid artery stenosis (BCAS) to investigate the role of B-cell translocation gene 2 (BTG2), an antiproliferation gene, in the white matter glial response to chronic cerebral hypoperfusion. [15] We investigated the role of B-cell translocation gene 1 (BTG1) in cystine and methionine deficiency (CST/Met (−))-mediated cell death. [16] Loss- and gain-function approaches were conducted to determine the roles of microRNA (miR)-146a, B-cell translocation gene 2 (BTG2), and Bcl-2-associated X protein (Bax) in post-operative effects on cognitive function and neuronal apoptosis. [17] Further, the genomic pattern according to MATH demonstrated that mutation rates of immunoglobulin lambda locus, B-cell translocation gene and membrane-associated guanylate kinase were the sites with the highest mutation rate. [18] The relation between B-cell translocation gene 1 (BTG1) and miR-330-3p was predicted by TargetScan and confirmed by dual-luciferase reporter assay. [19] Moreover, Dex-increased ATG7 expression and autophagy was mediated by enhanced expression of BTG1 (B cell translocation gene 1, anti-proliferative) that stimulated activity of CREB1 (cAMP response element binding protein 1). [20] B-cell translocation gene 1 (BTG1) is a member of the BTG/transducer of Erb family. [21] Mechanistically, B-cell translocation gene 3 (BTG3) was identified as a direct downstream target of miR-519c-3p. [22] Hypoxia-inducible factor-1α (HIF1α) and B-cell translocation gene 3 (BTG3) expressions were examined in oleuropein-treated EC cells. [23] B-cell translocation gene 1 (BTG1) has also been implicated with CRC. [24] In addition, our results indicated that NUSAP1 knockdown increased the gene expression of B‐cell translocation gene 2 (BTG2), but decreased the expression levels of phosphoinositide 3‐kinase (PI3K) and phosphorylated serine/threonine kinase (p‐AKT). [25] Expressions of nuclear receptor subfamily 2 group C member 2 (NR2C2), B cell translocation gene 2, T-box-19 (TBX19), and cyclin-dependent kinase 2 (CDK2) in surgically resected specimens were assessed by immunohistochemistry. [26] ST interacts with and inhibits the function of heterochromatin protein 1–binding protein 3 (HP1BP3), a positive regulator of global microRNA biogenesis, and it thereby triggers aberrant upregulation of B-cell translocation gene 2 (BTG2), which is essential for prevention of SASP and OIS by ST. [27] Mechanically, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) identified that HOTAIRM1 and B-cell translocation gene 3 (BTG3) were target genes of miR-17-5p. [28] Here we report that bioinformatics-based integrative analyses can assist in the study of mechanisms modulated by mechanical stress within OA pathology, and we reveal that B-cell Translocation Gene 2 (BTG2) can be a mechanosensitive gene involved in OA development. [29] Since the identification of B‐cell translocation gene 1 (BTG1) and BTG2 as antiproliferation genes more than two decades ago, their protein products have been implicated in a variety of cellular processes including cell division, DNA repair, transcriptional regulation and messenger RNA stability. [30] B-cell translocation gene 1 (BTG1), a translocation partner of the c-myc, is a tumor suppressor gene that promotes apoptosis and negatively regulates cellular proliferation and cell-to-cell adhesion. [31] In the present study, we report that Kruppel-like factor 15 (KLF15) is a novel mediator of b-cell translocation gene 2 (BTG2)-induced FGF21 biosynthesis. [32] A dual-luciferase reporter assay was performed to validate B-cell translocation gene 3 (BTG3) as a target of miR-20b-5p. [33] Background/Aim: The mechanism responsible for B-cell translocation gene 1 (BTG1) down-regulation in breast carcinoma remains unknown. [34] B cell translocation gene 1 (BTG1) works as a tumor suppressor in various cancer types. [35] Objective To investigate the expression of B cell translocation gene 3 (BTG3) in breast cancer tissues and its effect on proliferation and invasion of breast cancer cells. [36]B-세포 전위 유전자 2(BTG2)는 miR-365의 직접적인 표적으로 확인된 반면, 초점 접착 키나제(F/ATP) 의존성 티로신 키나제(AKT) 경로는 miR-365에 의해 활성화되었습니다. [1] CCR4-NOT 복합체의 어댑터 단백질인 B-세포 전위 유전자-4(Btg4)의 녹아웃은 수정 후 mRNA 붕괴 결함을 초래합니다. [2] 이 연구는 간세포암종 세포에서 해당과정과 세포자멸사를 조절하는 절단 및 폴리아데닐화 인자-6(CPSF6)과 B-세포 전위 유전자 2(BTG2)의 역할을 조사하는 것을 목표로 하고 있습니다. [3] nan [4] B-cell translocation gene 1(BTG1) mRNA는 miR-301a-3p의 새로운 표적으로 확인되었습니다. [5] nan [6] 목적: 이 연구에서 우리는 비소세포폐암(NSCLC) 환자의 예후를 예측하는 마커로서 혈장 엑소좀 유래 B-세포 전위 유전자 1(BTG-1) 수준을 조사하고자 했습니다. [7] nan [8] nan [9] 이중 루시퍼라제 리포터 분석은 miR-934가 B-세포 전위 유전자 2(BTG2)에 직접 결합함을 추가로 보여주었습니다. [10] nan [11] nan [12] nan [13] nan [14] nan [15] nan [16] nan [17] 또한, MATH에 따른 게놈 패턴은 면역글로불린 람다 유전자좌, B-세포 전위 유전자 및 막-연관 구아닐레이트 키나제의 돌연변이율이 가장 높은 돌연변이율을 갖는 부위임을 입증하였다. [18] B-세포 전위 유전자 1(BTG1)과 miR-330-3p 사이의 관계는 TargetScan에 의해 예측되었고 이중 루시퍼라제 리포터 분석에 의해 확인되었습니다. [19] 더욱이, Dex-증가된 ATG7 발현 및 자가포식은 CREB1(cAMP 반응 요소 결합 단백질 1)의 활성을 자극하는 BTG1(B 세포 전위 유전자 1, 항증식성)의 향상된 발현에 의해 매개되었다. [20] nan [21] 기계적으로, B-세포 전위 유전자 3(BTG3)은 miR-519c-3p의 직접적인 다운스트림 표적으로 확인되었습니다. [22] Hypoxia-inducible factor-1α (HIF1α)와 B-cell translocation gene 3 (BTG3)의 발현은 oleuropein 처리된 EC 세포에서 조사되었다. [23] nan [24] 또한, 우리의 결과는 NUSAP1 녹다운이 B-세포 전위 유전자 2(BTG2)의 유전자 발현을 증가시켰지만, 포스포이노시티드 3-키나제(PI3K) 및 인산화된 세린/트레오닌 키나제(p-AKT)의 발현 수준을 감소시키는 것으로 나타났습니다. [25] 외과적으로 절제된 표본에서 핵 수용체 서브패밀리 2 그룹 C 구성원 2(NR2C2), B 세포 전위 유전자 2, T-box-19(TBX19) 및 사이클린 의존성 키나제 2(CDK2)의 발현을 면역조직화학으로 평가했습니다. [26] nan [27] 기계적으로, 이중 루시퍼라제 리포터 분석 및 RNA 면역 침전(RIP)은 HOTAIRM1 및 B-세포 전위 유전자 3(BTG3)이 miR-17-5p의 표적 유전자임을 확인했습니다. [28] nan [29] nan [30] nan [31] nan [32] nan [33] nan [34] nan [35] nan [36]
Variant Translocation Gene
OBJECTIVE To detect the expression of long non-coding ribonucleic acid (lncRNA) plasmacytoma variant translocation gene 1 (PVT1) in uveal melanoma (UM) tissues, and to investigate its influence on the proliferation and apoptosis of UM cells as well as its mechanism. [1] Among the highly acknowledged lncRNAs is the human homolog of the plasmacytoma variant translocation gene, which is called PVT1. [2]목적 포도막 흑색종(UM) 조직에서 긴 비암호화 리보핵산(lncRNA) 형질세포종 변이 전위 유전자 1(PVT1)의 발현을 검출하고, UM 세포의 증식 및 세포 사멸에 미치는 영향 및 그 기전을 조사합니다. [1] 고도로 인정된 lncRNA 중에는 PVT1이라고 하는 형질세포종 변이 전위 유전자의 인간 상동체가 있습니다. [2]
Eleven Translocation Gene
Interestingly, the expression of TET1, a member of Ten-Eleven Translocation gene family for converting 5-methylcytosine (5 mC) to 5-hydroxymethylcytosine (5hmC), was decreased after EZH2 knockdown, in contrast to the increase of the other two members, TET2 and TET3 (P < 0. [1] TET2, a member of the Ten‐Eleven translocation gene family, catalyzes the conversion of 5‐methylcytosine to 5‐hydroxymethylcytosine in DNA. [2]흥미롭게도, 5-메틸시토신(5mC)을 5-하이드록시메틸시토신(5hmC)으로 전환하기 위한 Ten-Eleven Translocation 유전자 패밀리의 구성원인 TET1의 발현은 다른 두 구성원의 증가와 대조적으로 EZH2 녹다운 후 감소했습니다. TET2 및 TET3(P<0. [1] Ten-Eleven 전위 유전자 패밀리의 구성원인 TET2는 DNA에서 5-메틸시토신을 5-히드록시메틸시토신으로 전환하는 것을 촉매합니다. [2]
translocation gene 2 전좌 유전자 2
The translocation gene 2 section is under construction...translocation gene 1 전좌 유전자 1
B-cell translocation gene 1 (BTG1) mRNA was identified as the novel target of miR-301a-3p. [1] Objective: In this study, we wanted to investigate the plasma exosome-derived B-cell translocation gene 1 (BTG-1) level as a predictive marker for the prognosis in patients with Non-small cell lung cancer (NSCLC). [2] METHODS The expression levels of miR-183-5p and B-cell translocation gene 1 (Btg1) were determined by quantitative real-time PCR and histological analysis in livers of obese mice and cell models induced with palmitic acid (PA), respectively. [3] We previously showed that pulmonary mucosa-associated lymphoid tissue (MALT) lymphoma could be diagnosed by detecting MALT lymphoma translocation gene 1 (MALT1) translocations in bronchoalveolar lavage fluid (BALF) cells. [4] We investigated the role of B-cell translocation gene 1 (BTG1) in cystine and methionine deficiency (CST/Met (−))-mediated cell death. [5] The relation between B-cell translocation gene 1 (BTG1) and miR-330-3p was predicted by TargetScan and confirmed by dual-luciferase reporter assay. [6] Moreover, Dex-increased ATG7 expression and autophagy was mediated by enhanced expression of BTG1 (B cell translocation gene 1, anti-proliferative) that stimulated activity of CREB1 (cAMP response element binding protein 1). [7] B-cell translocation gene 1 (BTG1) is a member of the BTG/transducer of Erb family. [8] B-cell translocation gene 1 (BTG1) has also been implicated with CRC. [9] MALT1 (mucosa-associated lymphoid tissue lymphoma-translocation gene 1) is an intracellular signaling protein that activates NFκB and is crucial for both the adaptive and innate immune responses. [10] OBJECTIVE To detect the expression of long non-coding ribonucleic acid (lncRNA) plasmacytoma variant translocation gene 1 (PVT1) in uveal melanoma (UM) tissues, and to investigate its influence on the proliferation and apoptosis of UM cells as well as its mechanism. [11] Since the identification of B‐cell translocation gene 1 (BTG1) and BTG2 as antiproliferation genes more than two decades ago, their protein products have been implicated in a variety of cellular processes including cell division, DNA repair, transcriptional regulation and messenger RNA stability. [12] B-cell translocation gene 1 (BTG1), a translocation partner of the c-myc, is a tumor suppressor gene that promotes apoptosis and negatively regulates cellular proliferation and cell-to-cell adhesion. [13] Background/Aim: The mechanism responsible for B-cell translocation gene 1 (BTG1) down-regulation in breast carcinoma remains unknown. [14] B cell translocation gene 1 (BTG1) works as a tumor suppressor in various cancer types. [15]B-cell translocation gene 1(BTG1) mRNA는 miR-301a-3p의 새로운 표적으로 확인되었습니다. [1] 목적: 이 연구에서 우리는 비소세포폐암(NSCLC) 환자의 예후를 예측하는 마커로서 혈장 엑소좀 유래 B-세포 전위 유전자 1(BTG-1) 수준을 조사하고자 했습니다. [2] nan [3] nan [4] nan [5] B-세포 전위 유전자 1(BTG1)과 miR-330-3p 사이의 관계는 TargetScan에 의해 예측되었고 이중 루시퍼라제 리포터 분석에 의해 확인되었습니다. [6] 더욱이, Dex-증가된 ATG7 발현 및 자가포식은 CREB1(cAMP 반응 요소 결합 단백질 1)의 활성을 자극하는 BTG1(B 세포 전위 유전자 1, 항증식성)의 향상된 발현에 의해 매개되었다. [7] nan [8] nan [9] nan [10] 목적 포도막 흑색종(UM) 조직에서 긴 비암호화 리보핵산(lncRNA) 형질세포종 변이 전위 유전자 1(PVT1)의 발현을 검출하고, UM 세포의 증식 및 세포 사멸에 미치는 영향 및 그 기전을 조사합니다. [11] nan [12] nan [13] nan [14] nan [15]
translocation gene 3
Mechanistically, B-cell translocation gene 3 (BTG3) was identified as a direct downstream target of miR-519c-3p. [1] Hypoxia-inducible factor-1α (HIF1α) and B-cell translocation gene 3 (BTG3) expressions were examined in oleuropein-treated EC cells. [2] Mechanically, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) identified that HOTAIRM1 and B-cell translocation gene 3 (BTG3) were target genes of miR-17-5p. [3] A dual-luciferase reporter assay was performed to validate B-cell translocation gene 3 (BTG3) as a target of miR-20b-5p. [4] Objective To investigate the expression of B cell translocation gene 3 (BTG3) in breast cancer tissues and its effect on proliferation and invasion of breast cancer cells. [5]기계적으로, B-세포 전위 유전자 3(BTG3)은 miR-519c-3p의 직접적인 다운스트림 표적으로 확인되었습니다. [1] Hypoxia-inducible factor-1α (HIF1α)와 B-cell translocation gene 3 (BTG3)의 발현은 oleuropein 처리된 EC 세포에서 조사되었다. [2] 기계적으로, 이중 루시퍼라제 리포터 분석 및 RNA 면역 침전(RIP)은 HOTAIRM1 및 B-세포 전위 유전자 3(BTG3)이 miR-17-5p의 표적 유전자임을 확인했습니다. [3] nan [4] nan [5]
translocation gene 2 전좌 유전자 2
B‐cell translocation gene 2 (BTG2) was identified to be a direct target of miR‐365, while the focal adhesion kinase (F/ATP)‐dependent tyrosine kinase (AKT) pathway was activated by miR‐365. [1] This study aimed to investigate the role of cleavage and polyadenylation factor-6 (CPSF6) and B-cell translocation gene 2 (BTG2) in regulating the glycolysis and apoptosis in HCC cells. [2] B-cell translocation gene 2 (BTG2) and yin yang 1 (YY1) are key regulators of diverse metabolic processes. [3] This research aims to probe the protective effects of exosomal miR-150-5p from BMSCs on cerebral I/R injury via regulating B-cell translocation gene 2 (BTG2). [4] The current paper gives prominence to the role of miR-322-5p in MI by regulating B-cell translocation gene 2 (BTG2). [5] Dual luciferase reporter assay further showed that miR-934 directly bound to B-cell translocation gene 2 (BTG2). [6] Hence, this study intends to unearth the mechanism of AD, mainly focusing on miR-16-5p/B-cell translocation gene 2 (BTG2) axis. [7] A luciferase assay revealed that B-cell translocation gene 2 (BTG2) was a target gene of miR-15a and negatively correlated with miR-15a expression. [8] An ovalbumin-induced mouse asthma model was established, followed by injection of short hairpin RNA (sh)-EZH2, overexpression-B-cell translocation gene 2 (oe-BTG2), microRNA (miR)-34b agomir as well as their corresponding controls. [9] This review covers the following topics: tumor-promoting activity of the Tipα family members HP-MP1 and Tipα, the mechanism underlying this activity of Tipα via binding to the cell-surface receptor, nucleolin, the crystal structure of rdel-Tipα and N-terminal truncated rTipα, inhibition of Tipα-associated gastric carcinogenesis by tumor suppressor B-cell translocation gene 2 (BTG2/TIS21), and new strategies to prevent and treat gastric cancer. [10] In this study, we used a mouse model of bilateral common carotid artery stenosis (BCAS) to investigate the role of B-cell translocation gene 2 (BTG2), an antiproliferation gene, in the white matter glial response to chronic cerebral hypoperfusion. [11] Loss- and gain-function approaches were conducted to determine the roles of microRNA (miR)-146a, B-cell translocation gene 2 (BTG2), and Bcl-2-associated X protein (Bax) in post-operative effects on cognitive function and neuronal apoptosis. [12] In addition, our results indicated that NUSAP1 knockdown increased the gene expression of B‐cell translocation gene 2 (BTG2), but decreased the expression levels of phosphoinositide 3‐kinase (PI3K) and phosphorylated serine/threonine kinase (p‐AKT). [13] Expressions of nuclear receptor subfamily 2 group C member 2 (NR2C2), B cell translocation gene 2, T-box-19 (TBX19), and cyclin-dependent kinase 2 (CDK2) in surgically resected specimens were assessed by immunohistochemistry. [14] ST interacts with and inhibits the function of heterochromatin protein 1–binding protein 3 (HP1BP3), a positive regulator of global microRNA biogenesis, and it thereby triggers aberrant upregulation of B-cell translocation gene 2 (BTG2), which is essential for prevention of SASP and OIS by ST. [15] Here we report that bioinformatics-based integrative analyses can assist in the study of mechanisms modulated by mechanical stress within OA pathology, and we reveal that B-cell Translocation Gene 2 (BTG2) can be a mechanosensitive gene involved in OA development. [16] In the present study, we report that Kruppel-like factor 15 (KLF15) is a novel mediator of b-cell translocation gene 2 (BTG2)-induced FGF21 biosynthesis. [17]B-세포 전위 유전자 2(BTG2)는 miR-365의 직접적인 표적으로 확인된 반면, 초점 접착 키나제(F/ATP) 의존성 티로신 키나제(AKT) 경로는 miR-365에 의해 활성화되었습니다. [1] 이 연구는 간세포암종 세포에서 해당과정과 세포자멸사를 조절하는 절단 및 폴리아데닐화 인자-6(CPSF6)과 B-세포 전위 유전자 2(BTG2)의 역할을 조사하는 것을 목표로 하고 있습니다. [2] nan [3] nan [4] nan [5] 이중 루시퍼라제 리포터 분석은 miR-934가 B-세포 전위 유전자 2(BTG2)에 직접 결합함을 추가로 보여주었습니다. [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12] 또한, 우리의 결과는 NUSAP1 녹다운이 B-세포 전위 유전자 2(BTG2)의 유전자 발현을 증가시켰지만, 포스포이노시티드 3-키나제(PI3K) 및 인산화된 세린/트레오닌 키나제(p-AKT)의 발현 수준을 감소시키는 것으로 나타났습니다. [13] 외과적으로 절제된 표본에서 핵 수용체 서브패밀리 2 그룹 C 구성원 2(NR2C2), B 세포 전위 유전자 2, T-box-19(TBX19) 및 사이클린 의존성 키나제 2(CDK2)의 발현을 면역조직화학으로 평가했습니다. [14] nan [15] nan [16] nan [17]
translocation gene 1 전좌 유전자 1
The translocation gene 1 section is under construction...translocation gene family
The myeloid translocation gene family member MTG16 is a transcriptional corepressor that relies on the DNA-binding ability of other proteins to determine specificity. [1] Interestingly, the expression of TET1, a member of Ten-Eleven Translocation gene family for converting 5-methylcytosine (5 mC) to 5-hydroxymethylcytosine (5hmC), was decreased after EZH2 knockdown, in contrast to the increase of the other two members, TET2 and TET3 (P < 0. [2] TET2, a member of the Ten‐Eleven translocation gene family, catalyzes the conversion of 5‐methylcytosine to 5‐hydroxymethylcytosine in DNA. [3]골수성 전위 유전자 패밀리 구성원 MTG16은 특이성을 결정하기 위해 다른 단백질의 DNA 결합 능력에 의존하는 전사 공동 억제자입니다. [1] 흥미롭게도, 5-메틸시토신(5mC)을 5-하이드록시메틸시토신(5hmC)으로 전환하기 위한 Ten-Eleven Translocation 유전자 패밀리의 구성원인 TET1의 발현은 다른 두 구성원의 증가와 대조적으로 EZH2 녹다운 후 감소했습니다. TET2 및 TET3(P<0. [2] Ten-Eleven 전위 유전자 패밀리의 구성원인 TET2는 DNA에서 5-메틸시토신을 5-히드록시메틸시토신으로 전환하는 것을 촉매합니다. [3]