# SBK3

## Overview
SBK3, or SH3 domain binding kinase family member 3, is a gene that encodes a protein belonging to the kinase family known for interacting with the Src homology 3 (SH3) domain. This protein is categorized as a kinase due to its role in modulating intracellular signaling pathways, which are crucial for various cellular processes such as cell proliferation, differentiation, and apoptosis. The SBK3 gene is notably expressed in the atrial appendage of the human heart, suggesting a specialized function in cardiac tissues, although its precise biological roles remain to be fully elucidated (Ahn2020Integrative). The protein's interactions and pathways are not yet well-characterized, indicating a need for further research to understand its potential implications in both normal physiology and disease contexts.

## Function
SBK3 (SH3 domain binding kinase family member 3) is a protein-coding gene that is part of a group of kinases known to bind to the Src homology 3 (SH3) domain. This domain is involved in various cellular functions, including cell proliferation, cytoskeletal modifications, and signal transduction (Ahn2020Integrative). SBK3 is specifically expressed in the atrial appendage of the human heart, indicating a potential role in heart-specific functions, although its precise pathways and roles in healthy human cells remain to be fully elucidated (Ahn2020Integrative).

The protein encoded by SBK3 is likely active in the cytoplasm, where it interacts with other proteins to modulate intracellular signaling pathways. These interactions may influence processes such as cell growth, differentiation, and apoptosis. Despite its identification as an atrial appendage-specific gene, the specific molecular activities and organismal outcomes of SBK3's functions in the heart or other tissues have not been extensively characterized, highlighting the need for further research to understand its roles in cellular and physiological contexts (Ahn2020Integrative).

## Clinical Significance
SBK3 (SH3 domain binding kinase family member 3) has been implicated in several clinical contexts, although its specific roles and mechanisms remain under investigation. In the context of heart health, SBK3 is identified as an atrial appendage-specific gene, suggesting a potential role in heart-specific functions or conditions, though its exact pathways and clinical implications in cardiac health are not yet fully understood (Ahn2020Integrative).

In cancer research, SBK3 has been included in a prognostic model for hepatocellular carcinoma (HCC) associated with TP53 mutations. This model, which includes SBK3 among other genes, has been shown to predict patient prognosis, with higher expression levels correlating with poorer survival outcomes. This suggests that SBK3 may play a role in the progression or severity of HCC, although its specific contributions require further study (Yang2024Identification).

SBK3 has also been highlighted as a potential therapeutic target in centronuclear myopathies (CNM). It is part of a therapy signature identified in mouse models, and drugs targeting SBK3, such as nintedanib, are being explored for their therapeutic potential in CNM and possibly other diseases (Djeddi2021Multiomics).

## Interactions
SBK3 (SH3 domain binding kinase family member 3) is a protein that belongs to a group of kinases known for binding to the Src homology 3 (SH3) domain. This domain is involved in various cellular functions, including cell proliferation, cytoskeletal modifications, and signal transduction (Ahn2020Integrative). Despite its classification, specific pathways and interaction partners for SBK3 have not been identified in the studies reviewed. The role of SBK3 in the atrial appendage of the heart has been noted, but its specific interactions within this context remain unexplored (Ahn2020Integrative).

In the context of glioblastomas, SBK3 was evaluated for its ability to bind to an extracellular fragment of protein tyrosine phosphatase μ (PTPμ). However, SBK3 showed poor binding to glioblastoma tumors in vivo, indicating that it does not effectively interact with the PTPμ fragment in this setting (BurdenGulley2010A). This suggests that SBK3 may not participate in significant interactions with PTPμ in glioblastoma tissues.

Overall, while SBK3 is recognized as part of the SH3 domain binding kinase family, its specific interaction partners and roles in cellular processes are not well-documented and require further investigation.


## References


[1. (BurdenGulley2010A) Susan M. Burden-Gulley, Theresa J. Gates, Adam M. Burgoyne, Jennifer L. Cutter, David T. Lodowski, Shenandoah Robinson, Andrew E. Sloan, Robert H. Miller, James P. Basilion, and Susann M. Brady-Kalnay. A novel molecular diagnostic of glioblastomas: detection of an extracellular fragment of protein tyrosine phosphatase μ. Neoplasia, 12(4):305-IN2, April 2010. URL: http://dx.doi.org/10.1593/NEO.91940, doi:10.1593/neo.91940. This article has 48 citations and is from a domain leading peer-reviewed journal.](https://doi.org/10.1593/NEO.91940)

[2. (Djeddi2021Multiomics) Sarah Djeddi, David Reiss, Alexia Menuet, Sébastien Freismuth, Juliana de Carvalho Neves, Sarah Djerroud, Xènia Massana-Muñoz, Anne-Sophie Sosson, Christine Kretz, Wolfgang Raffelsberger, Céline Keime, Olivier M. Dorchies, Julie Thompson, and Jocelyn Laporte. Multi-omics comparisons of different forms of centronuclear myopathies and the effects of several therapeutic strategies. Molecular Therapy, 29(8):2514–2534, August 2021. URL: http://dx.doi.org/10.1016/j.ymthe.2021.04.033, doi:10.1016/j.ymthe.2021.04.033. This article has 14 citations and is from a highest quality peer-reviewed journal.](https://doi.org/10.1016/j.ymthe.2021.04.033)

[3. (Ahn2020Integrative) Jinsoo Ahn, Huiguang Wu, and Kichoon Lee. Integrative analysis revealing human heart-specific genes and consolidating heart-related phenotypes. Frontiers in Genetics, July 2020. URL: http://dx.doi.org/10.3389/fgene.2020.00777, doi:10.3389/fgene.2020.00777. This article has 7 citations and is from a peer-reviewed journal.](https://doi.org/10.3389/fgene.2020.00777)

[4. (Yang2024Identification) Qijun Yang, Lianke Gao, Yuhan Xu, Gaoquan Cao, Yingcheng He, Wenyige Zhang, Xue Zhang, Chengfeng Wu, Kaili Liao, and Xiaozhong Wang. Identification of tp53 mutation-associated prognostic genes and investigation of the immune cell infiltration in patients with hepatocellular carcinoma. Genes & Diseases, 11(2):520–523, March 2024. URL: http://dx.doi.org/10.1016/j.gendis.2023.03.020, doi:10.1016/j.gendis.2023.03.020. This article has 0 citations.](https://doi.org/10.1016/j.gendis.2023.03.020)