Ccn2a作用于cx43的下游,影响斑马鱼鳍再生过程中的关节形成。

IF 1.8 4区 生物学 Q3 BIOLOGY
Biology Open Pub Date : 2025-02-15 Epub Date: 2025-02-20 DOI:10.1242/bio.061674
Victoria Hyland, M Kathryn Iovine
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引用次数: 0

摘要

这项研究为斑马鱼鳍再生过程中骨骼模式的分子途径提供了新的见解。已知Connexin43 (Cx43)通过抑制evx1表达从而调节关节形成的时间来影响骨骼模式。在这里,我们通过证明细胞通信网络因子2 (ccn2a)也有助于这一途径,从而增加了这一途径。我们发现Ccn2a似乎作用于Cx43的下游,同样通过抑制evx1的表达来抑制关节的形成。β-catenin的药理抑制表明ccn2a可能受β-catenin的调控。此外,本文还提供了Yap信号通过调节ccn2a参与关节形成的证据。这些发现为Ccn2a在骨骼模式中的作用提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ccn2a acts downstream of cx43 to influence joint formation during zebrafish fin regeneration.

This study provides new insights into the molecular pathways dictating skeletal patterning during zebrafish fin regeneration. Connexin43 (Cx43) is known to influence skeletal patterning by inhibiting evx1 expression and thereby regulating the timing of joint formation. Here, we demonstrate that cellular communication network factor 2 (ccn2a) also contributes to this pathway. We find that Ccn2a appears to act downstream of Cx43 and similarly inhibits joint formation by inhibiting evx1 expression. Pharmacological inhibition of β-catenin demonstrates that ccn2a is likely regulated by β-catenin. Additionally, this paper provides evidence that Yap signaling contributes to joint formation through regulating ccn2a. These findings provide novel insights into the role of Ccn2a during skeletal patterning.

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来源期刊
Biology Open
Biology Open BIOLOGY-
CiteScore
3.90
自引率
0.00%
发文量
162
审稿时长
8 weeks
期刊介绍: Biology Open (BiO) is an online Open Access journal that publishes peer-reviewed original research across all aspects of the biological sciences. BiO aims to provide rapid publication for scientifically sound observations and valid conclusions, without a requirement for perceived impact.
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