Receptor Homolog(수용체 상동체)란 무엇입니까?
Receptor Homolog 수용체 상동체 - Few data are instead related to the role played by RON, a receptor homologous to MET. [1] aegypti sharing the most recent evolutionary origin sustain independence of function and signalling despite their relatively high degree of ligand and receptor homology. [2]MET와 상동인 수용체인 RON이 수행하는 역할과 관련된 데이터는 거의 없습니다. [1] 가장 최근의 진화적 기원을 공유하는 aegypti는 상대적으로 높은 수준의 리간드 및 수용체 상동성에도 불구하고 기능 및 신호 전달의 독립성을 유지합니다. [2]
orphan nuclear receptor 고아 핵 수용체
The orphan nuclear receptor, liver receptor homolog-1, is remodeled and reprogrammed in granulosa cells to direct global transcription during early ovulation for processes including cytoskeletal architecture and cell migration. [1] We demonstrate that, following the hormonal signal that initiates ovulation, granulosa cells undergo major modification of distal regulatory elements, which coincides with cistrome reprogramming of the indispensable orphan nuclear receptor liver receptor homolog-1 (LRH-1). [2] The orphan nuclear receptor liver receptor homolog-1 (LRH-1) serves prominent roles in malignancy; however, to the best of our knowledge, the role of LRH-1 in hepatoblastoma remains unknown. [3] LRH-1 (liver receptor homolog-1/NR5a2) is an orphan nuclear receptor, which regulates glucose and lipid metabolism, as well as intestinal inflammation via the transcriptional control of intestinal glucocorticoid synthesis. [4]고아 핵 수용체인 간 수용체 동족체-1은 세포골격 구조 및 세포 이동을 포함하는 과정을 위한 초기 배란 동안 전체 전사를 지시하기 위해 과립막 세포에서 리모델링 및 재프로그래밍됩니다. [1] 우리는 배란을 시작하는 호르몬 신호에 따라 과립막 세포가 필수 고아 핵 수용체 간 수용체 동족체-1(LRH-1)의 시스트롬 재프로그래밍과 일치하는 말단 조절 요소의 주요 수정을 겪는다는 것을 보여줍니다. [2] nan [3] nan [4]
diabetes nonalcoholic fatty 당뇨병 비알코올성 지방
The liver receptor homolog-1 (LRH-1, NR5A2), a member of the nuclear receptor superfamily, has emerged as a promising drug target for the treatment of diabetes, nonalcoholic fatty liver disease, inflammatory bowel disease, and cancers. [1] As a key regulator of metabolism and inflammation, the orphan nuclear hormone receptor, Liver Receptor Homolog-1 (LRH-1), has potential as a therapeutic target for diabetes, nonalcoholic fatty liver disease, and inflammatory bowel diseases. [2] As a key regulator of metabolism and inflammation, the orphan nuclear hormone receptor, Liver Receptor Homolog-1 (LRH-1), has potential as a therapeutic target for diabetes, nonalcoholic fatty liver disease, and inflammatory bowel diseases. [3]핵 수용체 슈퍼패밀리의 구성원인 간 수용체 동족체-1(LRH-1, NR5A2)은 당뇨병, 비알코올성 지방간 질환, 염증성 장 질환 및 암 치료를 위한 유망한 약물 표적으로 부상했습니다. [1] 신진대사 및 염증의 주요 조절자로서, 희귀 핵 호르몬 수용체인 간 수용체 동족체-1(LRH-1)은 당뇨병, 비알코올성 지방간 질환 및 염증성 장 질환의 치료 표적으로서 잠재력이 있습니다. [2] nan [3]
Liver Receptor Homolog 간 수용체 상동체
Liver receptor homolog‐1 (LRH‐1; NR5A2) is a nuclear receptor that regulates metabolic homeostasis in the liver. [1] We apply this new strategy to a panel of wild-type and mutant mice with a liver-specific gene deletion of Liver receptor homolog 1 (Lrh-1hep−/−), with both lines containing control individuals as well as individuals with liver cancer induced by diethylnitrosamine (DEN). [2] Steroidogenic factor-1 (SF-1)/adrenal 4-binding protein (Ad4BP)/NR5A1 and liver receptor homolog-1 (LRH-1) play important roles in these phenomena via transcriptional regulation. [3] Structures of phosphoinositide lipid binding proteins have also revealed new aspects of protein effector regulation, as mediated by the nuclear receptors Steroidogenic Factor-1 (SF-1, NR5A2) and Liver Receptor Homolog-1 (LRH-1, NR5A2). [4] Liver receptor homologue-1 (LRH-1) plays a critical role in hepatic metabolism and disease. [5] The orphan nuclear receptor, liver receptor homolog-1, is remodeled and reprogrammed in granulosa cells to direct global transcription during early ovulation for processes including cytoskeletal architecture and cell migration. [6] OBJECTIVE To explore the effect of geniposidic acid (GPA) on the signal pathway of small heterodimer dimer receptor (SHP) and liver receptor homologue 1 (LRH-1) in cholestasis rats induced by alpha-naphthalene isothiocyanate (ANIT). [7] The major targets identified for the herbs and spices compounds were dipeptidyl peptidase-4 (DPP4), intestinal maltase-glucoamylase (MGAM), liver receptor homolog-1 (NR5A2), pancreatic alpha-amylase (AM2A), peroxisome proliferator-activated receptor alpha (PPARA), protein tyrosine phosphatase non-receptor type 9 (PTPN9), and retinol binding protein-4 (RBP4) with over 250 compounds observed to be potential inhibitors of these particular protein targets. [8] The liver receptor homolog-1 (LRH-1, NR5A2), a member of the nuclear receptor superfamily, has emerged as a promising drug target for the treatment of diabetes, nonalcoholic fatty liver disease, inflammatory bowel disease, and cancers. [9] After 60 days of feeding, intestinal BA uptake and expression of apical sodium-dependent bile acid transporter (Asbt), organic solute transporter-alpha/beta (Osta/b) messenger RNA (mRNA), and hepatic expression of Na+ taurocholate cotransporting polypeptide (Ntcp), bile salt export pump (Bsep), cholesterol 7-α hydroxylase A1 (Cyp7a1), Farnesoid X receptor (Fxr), small heterodimer partner-1 (Shp), liver receptor homolog-1 (Lrh-1), and hepatic nuclear factor-4 alpha (Hnf4a) mRNA were measured. [10] Two of these, steroidogenic factor-1 (NR5A1, also known as SF-1) and liver receptor homolog-1 (NR5A2, also known as LRH-1), bind to the same DNA sequences, with different and nonoverlapping effects on targets. [11] As defective intestinal glucocorticoid synthesis has been associated with the development of IBD, we investigated the expression of steroidogenic enzymes and the key transcriptional regulator Liver Receptor Homolog-1 (LRH-1/NR5A2) in ileal and colonic biopsies human pediatric IBD and control patients. [12] In male C57/BL6 mice short term feeding of a Western diet (WD) resulted in increased glucocorticoid receptor expression in the ileum which was accompanied by an upregulation of the effector genes Sgk1 and sodium-hydrogen exchanger 3 (Nhe3) and liver receptor homologe 1 (Lrh1). [13] We demonstrate that, following the hormonal signal that initiates ovulation, granulosa cells undergo major modification of distal regulatory elements, which coincides with cistrome reprogramming of the indispensable orphan nuclear receptor liver receptor homolog-1 (LRH-1). [14] As a key regulator of metabolism and inflammation, the orphan nuclear hormone receptor, Liver Receptor Homolog-1 (LRH-1), has potential as a therapeutic target for diabetes, nonalcoholic fatty liver disease, and inflammatory bowel diseases. [15] The orphan nuclear receptor liver receptor homolog-1 (LRH-1) serves prominent roles in malignancy; however, to the best of our knowledge, the role of LRH-1 in hepatoblastoma remains unknown. [16] LRH-1 (liver receptor homolog-1/NR5a2) is an orphan nuclear receptor, which regulates glucose and lipid metabolism, as well as intestinal inflammation via the transcriptional control of intestinal glucocorticoid synthesis. [17] Overexpression of miR‐10a in hepatocytes blunted circadian rhythm of Bmal1 and inhibited the expression of lipid synthesis genes (sterol regulatory element binding protein [SREBP]1, fatty acid synthase [FASN], and SREBP2), gluconeogenesis (peroxisome proliferator‐activated receptor gamma coactivator 1 alpha [PGC1α]), protein synthesis (mammalian target of rapamycin [mTOR] and ribosomal protein S6 kinase [S6K]) and bile acid synthesis (liver receptor homolog 1 [LRH1]). [18] As a key regulator of metabolism and inflammation, the orphan nuclear hormone receptor, Liver Receptor Homolog-1 (LRH-1), has potential as a therapeutic target for diabetes, nonalcoholic fatty liver disease, and inflammatory bowel diseases. [19] De novo motif analysis identified colocalization of PXR with liver receptor homolog (LRH-1), which regulates bile acid synthesis after PCN exposure. [20]간 수용체 동족체-1(LRH-1; NR5A2)은 간에서 대사 항상성을 조절하는 핵 수용체입니다. [1] 우리는 이 새로운 전략을 간 수용체 동족체 1(Lrh-1hep-/-)의 간 특이적 유전자 결실이 있는 야생형 및 돌연변이 마우스 패널에 적용합니다. 두 라인 모두 대조군 개체와 간암 유발 개체를 포함합니다. 디에틸니트로사민(DEN)에 의해 [2] nan [3] nan [4] nan [5] 고아 핵 수용체인 간 수용체 동족체-1은 세포골격 구조 및 세포 이동을 포함하는 과정을 위한 초기 배란 동안 전체 전사를 지시하기 위해 과립막 세포에서 리모델링 및 재프로그래밍됩니다. [6] nan [7] nan [8] 핵 수용체 슈퍼패밀리의 구성원인 간 수용체 동족체-1(LRH-1, NR5A2)은 당뇨병, 비알코올성 지방간 질환, 염증성 장 질환 및 암 치료를 위한 유망한 약물 표적으로 부상했습니다. [9] nan [10] nan [11] nan [12] nan [13] 우리는 배란을 시작하는 호르몬 신호에 따라 과립막 세포가 필수 고아 핵 수용체 간 수용체 동족체-1(LRH-1)의 시스트롬 재프로그래밍과 일치하는 말단 조절 요소의 주요 수정을 겪는다는 것을 보여줍니다. [14] 신진대사 및 염증의 주요 조절자로서, 희귀 핵 호르몬 수용체인 간 수용체 동족체-1(LRH-1)은 당뇨병, 비알코올성 지방간 질환 및 염증성 장 질환의 치료 표적으로서 잠재력이 있습니다. [15] nan [16] nan [17] 간세포에서 miR-10a의 과발현은 Bmal1의 24시간 주기 리듬을 둔화시키고 지질 합성 유전자(스테롤 조절 요소 결합 단백질[SREBP]1, 지방산 합성 효소[FASN], SREBP2), 포도당 신생합성(peroxisome proliferator-activated receptor gamma)의 발현을 억제합니다. 보조 활성화제 1 알파[PGC1α]), 단백질 합성(라파마이신[mTOR] 및 리보솜 단백질 S6 키나아제[S6K]의 포유동물 표적) 및 담즙산 합성(간 수용체 동족체 1[LRH1]). [18] nan [19] nan [20]
Chemoattractant Receptor Homolog 화학 유인 수용체 상동체
Chemoattractant receptor homologous with T‐helper cell type 2 cells (CRTH2), a receptor for prostaglandin D2, is preferentially expressed on T‐helper cell type 2 lymphocytes, group 2 innate lymphoid cells, eosinophils, and basophils, and elicits the production of type 2 cytokines, including profibrotic IL‐13. [1] Hence, we investigate the potential effectiveness and underlying mechanism of CT-133, a newly developed selective antagonist of prostaglandin D2 receptor 2 (DP2) or of chemoattractant receptor homologous molecule expressed on Th2 cells (CRTH2), against lipopolysaccharide (LPS)-induced ALI. [2] Prostaglandin D2 and its cyclopentenone metabolites [cyclopentenone prostaglandins (CyPGs)], Δ12prostaglandin J2 and 15‐deoxy‐Δ12, 14‐prostaglandin J2, act through2GPCRs, d‐type prostanoid 1 and the chemoattractant receptor homologous molecule expressed on type 2 T‐helper cells (Crth2). [3] Inhibition of Th2 cells by chemoattractant receptor homologous molecule expressed on Th2 cells could suppress interleukin-4 and interleukin-13 secretion to reduce inflammation and thereby alleviate the elevated right ventricular systolic pressure and pulmonary vascular remodeling in rodent PAH models. [4] , leukotriene-synthesis inhibitors, CysLT-antagonists, and chemoattractant receptor homologous molecule on T-helper2-cells (CRTH2) antagonists] experienced drawbacks by lacking adequate biomarkers to define potential responders. [5]프로스타글란딘 D2 수용체인 T-helper cell type 2 세포와 상동성인 Chemoattractant receptor type 2 세포는 T-helper cell type 2 림프구, group 2 선천 림프구, 호산구, 호염기구에서 우선적으로 발현되며 type 의 생성을 유도합니다. profibrotic IL-13을 포함한 2개의 사이토카인. [1] 따라서 우리는 새로 개발된 프로스타글란딘 D2 수용체 2(DP2) 또는 Th2 세포에서 발현되는 화학유인 수용체 상동 분자(CRTH2)의 선택적 길항제인 CT-133의 지질다당류(LPS) 유도 ALI에 대한 잠재적 효과와 기본 메커니즘을 조사합니다. . [2] nan [3] nan [4] nan [5]
Cytocow Receptor Homolog Cytocow 수용체 상동체
All three major helices of isoform D interact with cytokine receptor homology (CRH) domain of the G-CSF receptor. [1] This receptor consists of an extracellular Ig-like domain, a cytokine receptor homology domain, 3 fibronectin domains, a trans-membrane domain, and a cytoplasmic domain that couples to Janus Kinases for signal transduction. [2] Most mutations occurred in the fibronectin III and cytokine receptor homology II domains, whereas none was found in cytoplasmic domain. [3]동형 D의 세 가지 주요 나선은 모두 G-CSF 수용체의 사이토카인 수용체 상동성(CRH) 도메인과 상호작용합니다. [1] 이 수용체는 세포외 Ig 유사 도메인, 사이토카인 수용체 상동성 도메인, 3개의 피브로넥틴 도메인, 막횡단 도메인 및 신호 전달을 위해 Janus Kinases에 결합하는 세포질 도메인으로 구성됩니다. [2] nan [3]
Insulin Receptor Homolog 인슐린 수용체 동족체
Results We found that expression of ATGL is increased in the insulin receptor homologue mutant daf-2 in a FoxO/DAF-16-dependent manner. [1] The brown planthopper (BPH) Nilaparvata lugens contains two insulin receptor homologues, designated NlInR1 and NlInR2. [2]결과 우리는 ATGL의 발현이 FoxO/DAF-16 의존적 방식으로 인슐린 수용체 상동 돌연변이 daf-2에서 증가한다는 것을 발견했습니다. [1] BPH(Brown planthopper) Nilaparvata lugens는 NlInR1 및 NlInR2로 지정된 두 개의 인슐린 수용체 동족체를 포함합니다. [2]
receptor homolog 1 수용체 상동체 1
We apply this new strategy to a panel of wild-type and mutant mice with a liver-specific gene deletion of Liver receptor homolog 1 (Lrh-1hep−/−), with both lines containing control individuals as well as individuals with liver cancer induced by diethylnitrosamine (DEN). [1] Overexpression of miR‐10a in hepatocytes blunted circadian rhythm of Bmal1 and inhibited the expression of lipid synthesis genes (sterol regulatory element binding protein [SREBP]1, fatty acid synthase [FASN], and SREBP2), gluconeogenesis (peroxisome proliferator‐activated receptor gamma coactivator 1 alpha [PGC1α]), protein synthesis (mammalian target of rapamycin [mTOR] and ribosomal protein S6 kinase [S6K]) and bile acid synthesis (liver receptor homolog 1 [LRH1]). [2]우리는 이 새로운 전략을 간 수용체 동족체 1(Lrh-1hep-/-)의 간 특이적 유전자 결실이 있는 야생형 및 돌연변이 마우스 패널에 적용합니다. 두 라인 모두 대조군 개체와 간암 유발 개체를 포함합니다. 디에틸니트로사민(DEN)에 의해 [1] 간세포에서 miR-10a의 과발현은 Bmal1의 24시간 주기 리듬을 둔화시키고 지질 합성 유전자(스테롤 조절 요소 결합 단백질[SREBP]1, 지방산 합성 효소[FASN], SREBP2), 포도당 신생합성(peroxisome proliferator-activated receptor gamma)의 발현을 억제합니다. 보조 활성화제 1 알파[PGC1α]), 단백질 합성(라파마이신[mTOR] 및 리보솜 단백질 S6 키나아제[S6K]의 포유동물 표적) 및 담즙산 합성(간 수용체 동족체 1[LRH1]). [2]