Golph3l-flox 基因敲除小鼠

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产品名称

Golph3l-flox 基因敲除小鼠

产品编号

S-CKO-07263

品系全称

C57BL/6JCya-Golph3lem1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-229593-Golph3l-B6J-VA

品系状态

使用本品系发表的文献需注明: Golph3l-flox 基因敲除小鼠 mice (Strain S-CKO-07263) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量
cKO小鼠库模型

基本信息

基因研究概述

质控标准

基因
基因全称
golgi phosphoprotein 3-like
基因别称
2010204I15Rik,Gpp34r
染色体号
Chr 3 (Mouse)
转录本 ID
NCBI: NM_146133 | Ensembl: ENSMUST00000177390
修饰方式
条件性基因敲除
靶向范围
Exon 3~4
敲除长度
~2.4 kb
品系说明
该品系是基于策略设计时的数据库信息制作而成,建议您在购买前查询最新的数据库和相关文献,以获取最准确的表型信息。
表型提示
GOLPH3L,全称Golgi phosphoprotein 3 like,是GOLPH3基因家族的一部分。GOLPH3L与GOLPH3基因相似,但它们的功能可能存在差异。GOLPH3L在多种生物学过程中发挥作用,包括细胞增殖、代谢和肿瘤发生。

GOLPH3L在乳腺癌中过表达,并且其表达水平与乳腺癌患者的预后相关。研究发现,敲低GOLPH3L可以抑制乳腺癌细胞的增殖、存活和迁移,并抑制肿瘤的生长。此外,GOLPH3L通过稳定p53诱导的SERPINE1,促进乳腺癌中的葡萄糖代谢[1]。在横纹肌肉瘤中,GOLPH3和GOLPH3L的表达增加,并且敲低这两种基因可以抑制横纹肌肉瘤细胞的增殖[2]。在卵巢癌中,GOLPH3L的表达显著上调,并且与卵巢癌患者的预后不良相关。GOLPH3L的过表达赋予卵巢癌细胞顺铂耐药性,而抑制GOLPH3L可以增强卵巢癌细胞对顺铂的敏感性。此外,GOLPH3L通过激活NF-κB信号通路促进卵巢癌细胞的耐药性[3]。在口腔鳞状细胞癌中,GOLPH3L是甲基化驱动基因之一,与患者的预后相关[4]。在精神分裂症中,GOLPH3L的表达与疾病状态相关,并且有遗传变异影响GOLPH3L的表达[5]。在皮肤和乳腺癌相关间变性大细胞淋巴瘤中,GOLPH3L的表达上调,并且与PI3K/AKT信号通路的激活相关[6]。在乳腺癌中,GOLPH3L是线粒体生物发生和翻译的标记之一,并且与患者的预后不良相关[7]。

综上所述,GOLPH3L在多种生物学过程中发挥作用,包括细胞增殖、代谢和肿瘤发生。GOLPH3L在乳腺癌、横纹肌肉瘤、卵巢癌、口腔鳞状细胞癌、精神分裂症和间变性大细胞淋巴瘤中表达上调,并且与这些疾病的预后相关。GOLPH3L的研究有助于深入理解其在生物学过程中的功能和疾病发生机制,为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Xu, Youqin, Chen, Wancheng, Liang, Jing, Chen, Wenxiao, Huang, Wenhua. 2021. The miR-1185-2-3p-GOLPH3L pathway promotes glucose metabolism in breast cancer by stabilizing p53-induced SERPINE1. In Journal of experimental & clinical cancer research : CR, 40, 47. doi:10.1186/s13046-020-01767-9. https://pubmed.ncbi.nlm.nih.gov/33509226/
2. Kunigou, Osamu, Nagao, Hiroko, Kawabata, Naoya, Komiya, Setsuro, Setoguchi, Takao. 2011. Role of GOLPH3 and GOLPH3L in the proliferation of human rhabdomyosarcoma. In Oncology reports, 26, 1337-42. doi:10.3892/or.2011.1413. https://pubmed.ncbi.nlm.nih.gov/21822541/
3. He, Shanyang, Niu, Gang, Shang, Jianhong, You, Zeshan, Shen, Hongwei. 2017. The oncogenic Golgi phosphoprotein 3 like overexpression is associated with cisplatin resistance in ovarian carcinoma and activating the NF-κB signaling pathway. In Journal of experimental & clinical cancer research : CR, 36, 137. doi:10.1186/s13046-017-0607-0. https://pubmed.ncbi.nlm.nih.gov/28978336/
4. Chen, Jun, Dong, Zejun, Li, Biaodong, Nie, Zhiliang, Qiu, Jiaxuan. 2024. Analysis of methylation-driven genes for predicting the prognosis of patients with oral squamous cell carcinoma. In Translational cancer research, 13, 2892-2904. doi:10.21037/tcr-23-2303. https://pubmed.ncbi.nlm.nih.gov/38988925/
5. Hauberg, Mads E, Fullard, John F, Zhu, Lingxue, Roeder, Kathryn, Roussos, Panos. 2018. Differential activity of transcribed enhancers in the prefrontal cortex of 537 cases with schizophrenia and controls. In Molecular psychiatry, 24, 1685-1695. doi:10.1038/s41380-018-0059-8. https://pubmed.ncbi.nlm.nih.gov/29740122/
6. Di Napoli, Arianna, Vacca, Davide, Bertolazzi, Giorgio, Berti, Emilio, Bhagat, Govind. 2021. RNA Sequencing of Primary Cutaneous and Breast-Implant Associated Anaplastic Large Cell Lymphomas Reveals Infrequent Fusion Transcripts and Upregulation of PI3K/AKT Signaling via Neurotrophin Pathway Genes. In Cancers, 13, . doi:10.3390/cancers13246174. https://pubmed.ncbi.nlm.nih.gov/34944796/
7. Sotgia, Federica, Whitaker-Menezes, Diana, Martinez-Outschoorn, Ubaldo E, Howell, Anthony, Lisanti, Michael P. 2012. Mitochondria "fuel" breast cancer metabolism: fifteen markers of mitochondrial biogenesis label epithelial cancer cells, but are excluded from adjacent stromal cells. In Cell cycle (Georgetown, Tex.), 11, 4390-401. doi:10.4161/cc.22777. https://pubmed.ncbi.nlm.nih.gov/23172368/