Pfdn1-KO 基因敲除小鼠

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产品名称

Pfdn1-KO 基因敲除小鼠

产品编号

S-KO-12160

品系全称

C57BL/6JCya-Pfdn1em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-67199-Pfdn1-B6J-VA

品系状态

使用本品系发表的文献需注明: Pfdn1-KO 基因敲除小鼠 mice (Strain S-KO-12160) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量

基本信息

基因研究概述

质控标准

基因
基因全称
prefoldin 1
基因别称
2700086I23Rik
染色体号
Chr 18 (Mouse)
转录本 ID
NCBI: NM_026027.3 | Ensembl: ENSMUST00000025204
修饰方式
全身性基因敲除
靶向范围
Exon 2
敲除长度
~167 bp
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
MGI:1914449Mice homozygous for a gene trapped allele display reduced birth size, slow weight gain, loss of neuron tracts in the brain, uncoordinated movement, impaired B and T cell development and function, mucus clearance defects, hydrocephaly, and premature deathpreceded by physical wasting.
PFDN1(Prefoldin subunit 1),也称为Prefoldin-1,是一种分子伴侣蛋白,参与细胞骨架的重组和蛋白质折叠过程。PFDN1属于Prefoldin家族,该家族的蛋白主要与细胞骨架的重排有关,并参与肿瘤进展等多种生物学过程。

PFDN1在多种肿瘤中表达上调,并与患者的预后不良相关。例如,在肝细胞癌(HCC)中,PFDN1的表达与肿瘤的进展和患者的预后不良相关[1]。PFDN1在胃癌(GC)中也被发现是一种不良预后的标记物[2]。此外,PFDN1在结直肠癌(CRC)和三阴性乳腺癌(TNBC)中的表达上调也与肿瘤的进展和患者的预后不良相关[3][4]。

PFDN1的表达上调可能通过多种机制促进肿瘤的进展。例如,PFDN1可以与细胞骨架蛋白如肌动蛋白和微管蛋白结合,从而影响细胞的增殖、迁移和侵袭[3]。PFDN1还可以影响细胞的细胞周期和凋亡,从而促进肿瘤的进展[4]。

除了在肿瘤中的作用外,PFDN1还与其他疾病相关。例如,PFDN1的表达与甲状腺功能和偏头痛相关[5][6]。此外,PFDN1还与阿尔茨海默病(AD)的结构改变相关[7]。

PFDN1在多种疾病中发挥重要作用,包括肿瘤、甲状腺功能、偏头痛和阿尔茨海默病。PFDN1的研究有助于深入理解细胞骨架重组和蛋白质折叠过程的生物学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. Ke, Shanjia, Lu, Shounan, Wang, Chaoqun, Wu, Yaohua, Ma, Yong. 2022. Comprehensive analysis of the prognostic value and functions of prefoldins in hepatocellular carcinoma. In Frontiers in molecular biosciences, 9, 957001. doi:10.3389/fmolb.2022.957001. https://pubmed.ncbi.nlm.nih.gov/36438659/
2. Yesseyeva, Galiya, Aikemu, Batuer, Hong, Hiju, Zheng, Minhua, Ma, Junjun. . Prefoldin subunits (PFDN1-6) serve as poor prognostic markers in gastric cancer. In Bioscience reports, 40, . doi:10.1042/BSR20192712. https://pubmed.ncbi.nlm.nih.gov/31957800/
3. Wang, Puxiongzhi, Zhao, Jingkun, Yang, Xiao, Lu, Aiguo, Zheng, Minhua. 2015. PFDN1, an indicator for colorectal cancer prognosis, enhances tumor cell proliferation and motility through cytoskeletal reorganization. In Medical oncology (Northwood, London, England), 32, 264. doi:10.1007/s12032-015-0710-z. https://pubmed.ncbi.nlm.nih.gov/26553318/
4. Alokda, Abdulrahman M, Soffar, Ahmed Abdelmagied, Yousef, Amany I, El-Sewedy, Tarek, Elmetwalli, Alaa. 2025. PFDN1 silencing disrupts critical cancer pathways in triple-negative breast cancer: investigating migration, cell cycle, and apoptosis as a new target therapy. In Naunyn-Schmiedeberg's archives of pharmacology, , . doi:10.1007/s00210-025-03975-6. https://pubmed.ncbi.nlm.nih.gov/40063241/
5. Tasnim, Sana, Wilson, Scott G, Walsh, John P, Nyholt, Dale R. . Shared genetics and causal relationships between migraine and thyroid function traits. In Cephalalgia : an international journal of headache, 43, 3331024221139253. doi:10.1177/03331024221139253. https://pubmed.ncbi.nlm.nih.gov/36739509/
6. Kwon, Mijung, Rubio, Genesaret, Wang, Haitao, Pine, Sharon R, Libutti, Steven K. 2022. Smoking-associated Downregulation of FILIP1L Enhances Lung Adenocarcinoma Progression Through Mucin Production, Inflammation, and Fibrosis. In Cancer research communications, 2, 1197-1213. doi:10.1158/2767-9764.CRC-22-0233. https://pubmed.ncbi.nlm.nih.gov/36860703/
7. Lu, Yingqi, Zhang, Xiaodong, Hu, Liyu, Chen, Shangjie, Xu, Jinping. 2024. Consistent genes associated with structural changes in clinical Alzheimer's disease spectrum. In Frontiers in neuroscience, 18, 1376288. doi:10.3389/fnins.2024.1376288. https://pubmed.ncbi.nlm.nih.gov/39554844/