basic FUNCTION
| inhibits both clathrin-dependent and clathrin-independent endocytic pathways by functionally sequestering dynamin via the SH3 domain of UBASH3A binding proline-rich sequences in dynamin |
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facilitates T-cell apoptosis independent of either T-cell receptor/CD3-mediated signaling or caspase activity |
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implicated in the regulation of signaling mediated by protein tyrosine kinases (PTKs) |
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with UBASH3B, may exert opposite effects on PTK-mediated signaling |
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function as critical negative regulators of TCR signaling |
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instrumental in down-modulating proteins that are dually modified by both protein tyrosine phosphorylation and ubiquitination |
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its phosphatase activity is key for its ability to negatively regulate the signaling of membrane-bound receptors including TCR and the epidermal growth factor receptor (EGFR) |
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might function as an acid-dependent phosphatase |
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UBASH3A, UBASH3B function as critical negative regulators of TCR signaling |
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suppressor of T-cell receptor signaling, underscoring antigen presentation to T-cells as a critical shared mechanism of diseases pathogenesis |
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UBASH3A can be considered as a common genetic factor in autoimmune diseases |
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suppress T-cell-driven inflammatory responses |
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may involve in the pathogenesis of Systemic Lupus Erythematosus (SLE) |
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pivotal role of UBASH3A/UBASH3B in regulating hematopoietic stem and progenitor cell fitness |
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UBASH3A attenuates the NFKB1 signal transduction upon T-cell receptor (TCR) stimulation by specifically suppressing the activation of the IKB kinase complex |
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is a negative regulator of NFKB1 signaling |
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CRKL, UBASH3A, and AIFM3 were detected in all phases of kidney development which implies their role as renal development control genes |