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糖皮質素受體

本頁使用了標題或全文手工轉換
維基百科，自由的百科全書
糖皮質素受體
已知的結構
PDB直系同源搜尋: PDBe RCSB
識別號
別名NR3C1；, GCCR, GCR, GCRST, GR, GRL, nuclear receptor subfamily 3 group C member 1, Glucocorticoid Receptor
外部IDOMIM：138040 MGI：95824 HomoloGene：30960 GeneCards：NR3C1
相關疾病
glucocorticoid resistance[1]
為以下藥物的標靶
莫米松、​去炎松、​潑尼松龍[2]
布地奈德、​環索奈德、​丙酸氯倍他索、​皮質醇、​11-去氧皮質酮、​去羥米松、​地塞米松、​difluprednate、​氟輕鬆、​氟欣諾能、​fluorometholone、​氟替卡松、​丙酸氟替卡松、​甲潑尼龍、​潑尼松龍、​強的松、​RU28362、​去炎松、​曲安奈德、​倍他米松、​美服培酮[3]
基因位置（人類）
5號染色體
染色體5號染色體[4]
5號染色體
糖皮質素受體的基因位置
糖皮質素受體的基因位置
基因座5q31.3起始143,277,931 bp[4]
終止143,435,512 bp[4]
RNA表現模式




查閱更多表現資料
直系同源
物種人類小鼠
Entrez

2908

14815

Ensembl

ENSG00000113580

ENSMUSG00000024431

UniProt

P04150
Q3MSN4

P06537

mRNA​序列

NM_008173
​NM_001361209
​NM_001361210
​NM_001361211
​NM_001361212

蛋白序列

NP_001348138
​NP_001348139
​NP_001348140
​NP_001348141
​NP_032199

基因位置​（UCSC）Chr 5: 143.28 – 143.44 MbChr 18: 39.54 – 39.65 Mb
PubMed​查找[6][7]
維基資料
檢視/編輯人類檢視/編輯小鼠

糖皮質素受體（英語：Glucocorticoid receptor, GR），也稱為NR3C1（核受體亞家族3，C組，成員1），是皮質醇和其他糖皮質素結合的受體。[8]

GR幾乎在身體的每個細胞中都有表現，並調節控制發育、新陳代謝和免疫反應的基因。因為受體基因以多種形式表現，它在身體的不同部位有許多不同的（多效性）作用。[9]

當糖皮質素與GR結合時，其主要作用機制是調節基因轉錄。[10]未結合的受體存在於細胞的胞質溶膠中。受體與糖皮質素結合後，受體-糖皮質素複合物可以採取兩種途徑中的任一種。活化的GR複合物上調細胞核中抗發炎蛋白的表現或抑制胞質溶膠中促炎蛋白的表現（通過阻止其他轉錄因子從細胞質轉移到細胞核中）。[11]

在人體內，GR蛋白由位於5號染色體上的NR3C1基因編碼。[12][13]

結構

與其他類固醇受體一樣，[14]糖皮質素受體在結構上是模塊化的，[15]並包含以下結構域（標記為A - F）：

  • A/B - N端調控域
  • C - DNA結合域（DBD）
  • D - 鉸鏈區
  • E - 配體結合域（LBD）
  • F - C端結構域

配體結合和反應

在沒有激素的情況下，糖皮質素受體位於與多種蛋白質複合的細胞質中，包括熱休克蛋白90（Hsp90）、熱休克蛋白70（Hsp70）和蛋白FKBP4（FK506結合蛋白4）。[16]內源性糖皮質素皮質醇通過細胞膜擴散到細胞質中並與糖皮質素受體結合，導致熱休克蛋白釋放。所得的活化形式GR具有兩種主要的作用機制，反式活化和反式阻遏，[17][18]如下所述。

轉錄活化

一種直接的作用機制包括受體的同二聚化、通過主動轉運進入細胞核的易位以及與活化基因轉錄的特定 DNA 反應元件的結合。該作用機制被稱為轉錄活化。生物反應取決於細胞類型。

轉錄抑制

在沒有活化的GR的情況下，其他轉錄因子如NF-κB或AP-1本身能夠反式活化靶基因。[19]

臨床意義

GR在家族性糖皮質素抵抗中異常。[20]

在中樞神經系統結構中，糖皮質素受體作為神經內分泌整合的新代表引起了人們的興趣，作為內分泌影響的主要成分。該受體現在與對壓力源的短期和長期適應有關，可能對理解心理障礙至關重要，包括部分或所有亞型抑鬱症和創傷後應激障礙（PTSD）。[21]庫欣病典型的情緒失調等長期觀察結果證明了皮質類固醇在調節心理狀態中的作用。最近的進展表明在神經水平上與正腎上腺素和血清素的相互作用。[22][23]

在先兆子癇（一種常見於孕婦的高血壓疾病）中，可能靶向該蛋白質的miRNA序列水平在母親的血液中升高。相反，胎盤提高了含有這種miRNA的外泌體的水平，可能導致分子轉譯的抑制。該資訊的臨床意義尚未明確。[24]

促效劑和拮抗劑

地塞米松和其他皮質類固醇是促效劑，[25]而米非司酮和酮康唑是GR的拮抗劑。[26]

相互作用

糖皮質素受體與以下物質相互作用：

研究

2022年6月28日發表的一篇論文表明，NR3C1可能是肌萎縮側索硬化（ALS）的潛在靶點之一。使用支持AI的生物靶點發現平台，發現NR3C1在CNS fALS和sALS中均被上調。通過靶點發現，可以進一步設計多種途徑和藥物來治療ALS。[64]

參考文獻

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