全世界約有15-20%的夫妻為此健康問題所困擾著，其中有一半是男性所導致的不孕。而LRWD1為實驗室利用正常人與造精功能障礙者（MA、SCOS）的睪丸組織，以cDNA microarray分析找出的基因，此基因的功能序列在真核生物中，具有相當高的保守性，因此LRWD1基因在真核生物中是非常重要的。
本實驗主要目的為研究LRWD1基因是否受NF-κB調控和LRWD1與centrosome的相關性。首先，利用WWW Promoter Scan預測人類LRWD1啟動子區域位，在-198~+100之間有可能的transcription factor binding sites，藉由ChIP assay確認NF-κB結合到LRWD1啟動子。以LPS活化NF-κB，結果磷酸化p65從細胞質移入細胞核的表現量上升。以LPS長時間處理細胞，使得下游LRWD1 RNA有增加的趨勢，以處理8小時表現量為最高。同樣以LPS處理長時間處理，以Western blot分析，40分鐘~1小時磷酸化p65表現量為最高；處理8小時，LRWD1表現量為最高。而BAY 11-7082會影響NF-κB的活化，進一步影響到下游LRWD1蛋白的製造。綜合以上研究結果顯示LRWD1啟動子確實受到轉錄因子NF-κB的調控。 It is estimated that 15-20% of couples are infertile and male factors account for about half of the cases. Leucine-rich Repeats and WD repeat Domain containing 1 (LRWD1) gene was originally identified by cDNA microarray as one of the genes down-regulated in the testicular tissues of patients with severe spermatogenic defects. The LRWD1 is very high levels of conservation among higher eukaryotes, with maximum homology discernible at the LRR- and WD-containing regions.
In the present study, LRWD1 gene is regulated by NF-κB and LRWD1 correlation with the centrosome. Use WWW Promoter Scan predicted human LRWD1 promoter region. Chromatin immune precipitation assay indicated that the p65 was binding in LRWD1 promoter. The binding activity was stimulated by LPS and inhibited by BAY 11-7082 treatments.
