Publications by authors named "Nasir Haider"
β-catenin has influential roles affecting embryonic development, tissue homeostasis, and human diseases including cancer. Cellular β-catenin levels are exquisitely controlled by a variety of regulatory mechanisms. In the course of exploring the functions of the Nek10 tyrosine kinase, we observed that deletion of Nek10 in lung adenocarcinoma cells resulted in dramatic stabilization of β-catenin, suggestive of a Nek10 role in the control of β-catenin turnover.
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- In response to DNA damage, various kinase signaling pathways activate the tumor suppressor p53, which manages the cellular response to such damage.
- Missing or faulty DNA damage response (DDR) pathways lead to increased mutations and risk for tumors, with recent studies highlighting the role of the NEK family of kinases, particularly NEK10, in this process.
- NEK10 enhances p53’s activity by specifically phosphorylating it at Y327; without NEK10, cells grow faster and are more vulnerable to DNA damage, while a combination of NEK10 and p53 target gene expression can predict better outcomes in breast cancer cases.
Article Synopsis
- Human NimA-related kinases (Neks) have various functions in cell division and other processes, but their specific substrates are still not well understood.* -
- Researchers identified the phosphorylation-site motifs across most of the Nek kinases, revealing differences in substrate preference, particularly distinguishing between serine and threonine acceptance and certain residue preferences.* -
- Nek10 stands out as a dual-specificity kinase that can phosphorylate both serine and tyrosine, with its mechanism influenced by unique residues, while Nek6, Nek7, and Nek9 have similar motifs to their activator Plk1, indicating they amplify Plk1's signaling.*
Early studies in lower Eukaryotes have defined a role for the members of the NimA related kinase (Nek) family of protein kinases in cell cycle control. Expansion of the Nek family throughout evolution has been accompanied by their broader involvement in checkpoint regulation and cilia biology. Moreover, mutations of Nek family members have been identified as drivers behind the development of ciliopathies and cancer.
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