# TEC (gene)
**TEC** (tec protein tyrosine kinase; also known as PSCTK4) is a human protein-coding gene on chromosome 4 that encodes a non-receptor tyrosine kinase of the TEC family, named for tyrosine kinase expressed in hepatocellular carcinoma, where the kinase was first identified in 1990.[1](https://www.ncbi.nlm.nih.gov/gene/7006) • [2](https://pubmed.ncbi.nlm.nih.gov/2284097/) The kinase participates in [T cell](https://www.edgepedia.org/t-cell) signaling and participates in intracellular signaling downstream of cytokine receptors, lymphocyte surface antigens, heterotrimeric G-protein-coupled receptors, and integrins.[1](https://www.ncbi.nlm.nih.gov/gene/7006)
| Key fact | Detail |
|---|---|
| Gene | TEC, HGNC 11719, Gene ID 7006, MIM 600583; protein coding, 20 exons, located at 4p12-p11 on chromosome 4[1](https://www.ncbi.nlm.nih.gov/gene/7006) |
| Discovery | Cloned in 1990 from a murine liver cDNA library screened with a v-fps kinase domain probe; highly expressed in 2 of 4 human hepatocellular carcinoma cell lines versus normal liver[2](https://pubmed.ncbi.nlm.nih.gov/2284097/) |
| Family | One of five mammalian TEC-family kinases: TEC, BTK, ITK, BMX/ETK, and TXK/RLK[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC5482768/) |
| Domain architecture | C-terminal tyrosine kinase domain, SH2 and SH3 protein-binding domains, and an N-terminal pleckstrin homology (PH) domain that binds the PI3K lipid product PIP3[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC5482768/) |
| Activation | PI3K-dependent recruitment to the plasma membrane via PIP3, followed by phosphorylation by other non-receptor tyrosine kinases; TEC activation is AKT-independent[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC5482768/) |
| Expression | Ubiquitous, with highest recorded expression in bone marrow (RPKM 2.4) and esophagus (RPKM 1.4); Tec and Bmx are the family members also found in endothelial cells[1](https://www.ncbi.nlm.nih.gov/gene/7006) • [4](https://pubmed.ncbi.nlm.nih.gov/17383541/) |
| Disease links | Possible association with myelodysplastic syndrome; TXK/TEC loci linked to rheumatoid arthritis[1](https://www.ncbi.nlm.nih.gov/gene/7006) • [5](https://febs.onlinelibrary.wiley.com/doi/10.1111/j.1742-4658.2011.08134.x) • [17](https://pubmed.ncbi.nlm.nih.gov/15188455/) |
## Discovery and gene structure
TEC was the founding member of its kinase family. In 1990, [Hiroyuki Mano](https://www.edgepedia.org/hiroyuki-mano) and colleagues at the [University of Tokyo](https://www.edgepedia.org/university-of-tokyo) screened a murine liver cDNA library with the v-fps kinase domain as a probe to find tyrosine kinases involved in hepatocarcinogenesis, and isolated cDNAs encoding a novel kinase they named tec, for tyrosine kinase expressed in hepatocellular carcinoma. The predicted protein's C-terminal domain showed significant homology to members of the src family, and Northern analysis showed the tec gene highly expressed in 2 of 4 human hepatocellular carcinoma cell lines compared with normal human liver.[2](https://pubmed.ncbi.nlm.nih.gov/2284097/) • [6](https://www.sciencedirect.com/science/article/abs/pii/S095279150200345X)
The human gene sits at 4p12-p11 on chromosome 4, spans 20 exons, and is cataloged as HGNC 11719 with Gene ID 7006 and MIM 600583; its official full name is tec protein tyrosine kinase and its alias is PSCTK4.[1](https://www.ncbi.nlm.nih.gov/gene/7006) NCBI records ubiquitous expression, with the highest levels in bone marrow (RPKM 2.4) and esophagus (RPKM 1.4).[1](https://www.ncbi.nlm.nih.gov/gene/7006)
## The TEC kinase family
TEC belongs to a five-member family of non-receptor (cytoplasmic) protein tyrosine kinases that also includes BTK (Bruton's tyrosine kinase), ITK (interleukin-2-inducible T-cell kinase), BMX (bone marrow tyrosine kinase gene on chromosome X, also known as ETK), and TXK (also known as RLK).[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC5482768/) Tec kinases constitute the second largest family of cytoplasmic protein tyrosine kinases and are expressed predominantly in hematopoietic cells, with Tec and Bmx also found in endothelial cells.[4](https://pubmed.ncbi.nlm.nih.gov/17383541/) The family evolved roughly 600 million years ago, before the existence of metazoans.[5](https://febs.onlinelibrary.wiley.com/doi/10.1111/j.1742-4658.2011.08134.x)
**Shared architecture.** In every one of the five proteins, a C-terminal tyrosine kinase domain sits downstream of SH2 and SH3 modules that mediate protein binding; all but TXK also carry an N-terminal PH domain, which recognizes PIP3, the phosphatidylinositol-3,4,5-trisphosphate generated by PI3K.[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC5482768/) Binding of PIP3 accumulates TEC, BMX, BTK, and ITK at the plasma membrane, where they are phosphorylated and activated by other non-receptor tyrosine kinases. This makes TEC-family activation dependent on PI3K signaling, in contrast to SRC family kinases, which are tethered to membranes constitutively by myristoyl and palmitoyl lipid modifications; TEC kinase activation is AKT-independent even when PI3K simultaneously activates AKT in the same cell.[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC5482768/) Structural work on an ancestral TEC kinase from the choanoflagellate *Monosiga brevicollis* shows that PIP3 relieves autoinhibition by displacing the PH domain from a conserved intramolecular contact with the kinase domain, and that PIP3 is necessary but not sufficient for activation.[7](https://www.nature.com/articles/s44511-026-00001-z)
## Signaling roles
Tec family kinases participate in the intracellular signaling of cytokine receptors, lymphocyte surface antigens, heterotrimeric G-protein-coupled receptors, and integrin molecules.[8](https://pubmed.ncbi.nlm.nih.gov/10647781/) In lymphocytes, three family members, ITK, RLK, and TEC, are expressed in T cells and activated in response to T cell receptor engagement, contributing to regulation of phospholipase C-γ, calcium mobilization, and mitogen-activated protein kinase activation.[9](https://www.nature.com/articles/nri1591) Across these systems, Tec family kinases are not essential signaling components but function to modulate or amplify signaling pathways; mutations that eliminate them quantitatively reduce proximal signaling yet qualitatively alter T cell development and differentiation.[10](https://www.annualreviews.org/content/journals/10.1146/annurev.immunol.22.012703.104743)
**Expression in lymphocytes.** Tec expression in primary T and B cells is low compared with ITK and BTK, but Tec is up-regulated following T-cell activation and in T helper 1 and T helper 2 cells.[11](https://pmc.ncbi.nlm.nih.gov/articles/PMC355844/) Overexpression of Tec kinase in a Jurkat T cell line induces NFAT activation.[12](https://pure.eur.nl/ws/files/30144231/150736jasperripfinal_pdf_ridderprint.pdf)
**Role in B cells.** Although BTK's role in B cells has been studied extensively, TEC's role there remained unclear for years. A 2017 study found that TEC is not essential for normal [B cell](https://www.edgepedia.org/b-cell) development when BTK is present, but Tec-deficient mature B cells showed increased activation, proliferation, and survival upon B cell receptor stimulation, with significantly increased activation of the Akt/S6 kinase pathway even though PLCγ phosphorylation and calcium influx were unaffected. In Tec-deficient mice, B cell responses to model antigens and humoral immunity during influenza infection were enhanced, and aged mice lacking Tec developed a mild autoimmune phenotype. The authors concluded that in mature B cells, Tec and Btk may compete for activation of the Akt pathway, with Btk's activating capacity limited by the presence of Tec.[13](https://pubmed.ncbi.nlm.nih.gov/28275136/) Mice lacking both Tec and Btk show severe B cell deficiency, indicating redundant functions in B cell development and activation.[14](https://pmc.ncbi.nlm.nih.gov/articles/PMC2193106/)
## Disease associations and pharmacology
In human [extraskeletal myxoid chondrosarcoma](https://www.edgepedia.org/extraskeletal-myxoid-chondrosarcoma), the t(3;9) translocation creates a fusion of the nuclear receptor gene NR4A3 (also known as CHN or TEC) to the partner gene TFG, and the fusion product encodes a transcriptional activator more potent than NR4A3 itself.[1](https://www.ncbi.nlm.nih.gov/gene/7006) • [17](https://pubmed.ncbi.nlm.nih.gov/15188455/) The gene may also be associated with myelodysplastic syndrome, and recent GeneRIF entries report that TEC kinase stabilizes PLK4 to promote liver cancer metastasis.[1](https://www.ncbi.nlm.nih.gov/gene/7006) In a genome-wide screen, the TXK/TEC loci were associated with the development of rheumatoid arthritis.[5](https://febs.onlinelibrary.wiley.com/doi/10.1111/j.1742-4658.2011.08134.x)
**Drug selectivity.** TEC matters clinically as an off-target of BTK inhibitors. Ibrutinib, the first FDA-approved BTK inhibitor, carries off-target liabilities associated with adverse events including inhibition of EGFR (skin rash), TEC (bleeding), and CSK (atrial fibrillation).[15](https://pubs.acs.org/aptsfn/article/8/12/4312/3760958/An-Assessment-of-Kinase-Selectivity-Enzyme) Second-generation inhibitors have sought to limit such off-target profiles; in a head-to-head kinase panel evaluation, zanubrutinib showed preferential inhibition of BTK over TEC.[15](https://pubs.acs.org/aptsfn/article/8/12/4312/3760958/An-Assessment-of-Kinase-Selectivity-Enzyme) • [16](https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2021.630942/pdf) Reported IC50 values for TEC-family kinases vary widely across agents and assays; for example, published values for spebrutinib inhibition of ITK differ by more than an order of magnitude between studies.[16](https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2021.630942/pdf)
## References
1. [TEC tec protein tyrosine kinase [Homo sapiens], NCBI Gene](https://www.ncbi.nlm.nih.gov/gene/7006)
2. [Mano H et al. (1990). A novel protein-tyrosine kinase, tec, is preferentially expressed in liver. Oncogene 5:1781-6.](https://pubmed.ncbi.nlm.nih.gov/2284097/)
3. [PI3K Signaling in Cancer: Beyond AKT, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC5482768/)
4. [Felices M et al. (2007). Tec kinases in T cell and mast cell signaling. Adv Immunol 93:145-84.](https://pubmed.ncbi.nlm.nih.gov/17383541/)
5. [Hussain A et al. (2011). TEC family kinases in health and disease. The FEBS Journal.](https://febs.onlinelibrary.wiley.com/doi/10.1111/j.1742-4658.2011.08134.x)
6. [New insights into the regulation and functions of Tec family tyrosine kinases in the immune system, Immunology Today (ScienceDirect)](https://www.sciencedirect.com/science/article/abs/pii/S095279150200345X)
7. [Mechanism of activation of an ancestral TEC kinase by PIP3, npj Structural Biology (2026)](https://www.nature.com/articles/s44511-026-00001-z)
8. [Mano H (1999). Tec family of protein-tyrosine kinases: an overview of their structure and function. Cytokine Growth Factor Rev 10:267-80.](https://pubmed.ncbi.nlm.nih.gov/10647781/)
9. [TEC-family kinases: regulators of T-helper-cell differentiation, Nature Reviews Immunology](https://www.nature.com/articles/nri1591)
10. [Berg LJ et al. (2005). TEC family kinases in T lymphocyte development and function. Annual Review of Immunology 23:549-600.](https://www.annualreviews.org/content/journals/10.1146/annurev.immunol.22.012703.104743)
11. [Expression and Function of Tec, Itk, and Btk in Lymphocytes: Evidence for a Unique Role for Tec, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC355844/)
12. [Distinct and overlapping functions of TEC kinase and BTK in B cell receptor signaling (thesis, Erasmus University)](https://pure.eur.nl/ws/files/30144231/150736jasperripfinal_pdf_ridderprint.pdf)
13. [de Bruijn MJW et al. (2017). Distinct and Overlapping Functions of TEC Kinase and BTK in B Cell Receptor Signaling. J Immunol.](https://pubmed.ncbi.nlm.nih.gov/28275136/)
14. [Severe B Cell Deficiency in Mice Lacking the Tec Kinase Family Members Tec and Btk, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC2193106/)
15. [An Assessment of Kinase Selectivity, Enzyme Inhibition Kinases and in Vitro Activity for Several Bruton Tyrosine Kinase (BTK) Inhibitors, ACS Pharmacology & Translational Science (2025)](https://pubs.acs.org/aptsfn/article/8/12/4312/3760958/An-Assessment-of-Kinase-Selectivity-Enzyme)
16. [Comparative Analysis of BTK Inhibitors and Mechanisms Underlying Adverse Effects, Frontiers in Cell and Developmental Biology (2021)](https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2021.630942/pdf)
17. [pubmed.ncbi.nlm.nih.gov](https://pubmed.ncbi.nlm.nih.gov/15188455/)
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*Topic: Encyclopedia › Life and health › Biological foundations › Biochemistry and metabolism › Protein families and complexes › Kinase and phosphatase families › Protein kinase families › Protein tyrosine kinases › Tec-family kinases*
*Initially written Sep 17, 2026 · Reviewed: Oct 21, 2026 · Edited: Oct 15, 2026; Oct 21, 2026 · Last review: Oct 21, 2026*
*Copyright 2026 EdgeChat AI, a subsidiary of Biostate AI.*
License: Edgepedia Community License 1.0, https://www.edgepedia.org/edgepedia/license