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FLT3 (show FLT3 Proteins) has a role in cytarabine transport by SLC29A1 (show SLC29A1 Proteins) in pediatric acute leukemia
Data indicate a pathway MYSM1 (show MYSM1 Proteins)/miR (show MLXIP Proteins)-150/FLT3 (show FLT3 Proteins) that inhibits proliferation of B1a cells, which may be involved in the pathogenesis of systemic lupus erythematosus (SLE).
findings confirm that FLT3 (show FLT3 Proteins)-ITD-location influences disease biology and leads to changes in global gene expression. In our model, ITD-location alters proliferative capacity and sensitivity to FLT3 (show FLT3 Proteins)-TKI-treatment in vivo
a decision analysis comparing allo-HCT vs chemotherapy in first complete remission for patients with cytogenetically intermediate-risk acute myeloid leukemia (show BCL11A Proteins), depending on the presence or absence of FLT3 (show FLT3 Proteins)-ITD), NPM1 (show NPM1 Proteins), and CEBPA (show CEBPA Proteins) mutations showed that allo-HCT was a favored postremission strategy in patients with FLT3 (show FLT3 Proteins)-ITD, and chemotherapy was favored in patients with biallelic CEBPA (show CEBPA Proteins) mutations.
ATM (show ATM Proteins)/G6PD (show G6PD Proteins)-driven redox metabolism promotes FLT3 (show FLT3 Proteins) inhibitor resistance in acute myeloid leukemia (show BCL11A Proteins) that can be successfully reversed.
Data suggest that there is a place for escalated daunorubicin dosing for fms-like tyrosine kinase 3 (FLT3 (show FLT3 Proteins))-ITD mutated cases.
Integrin alphavbeta3 (show ITGAV Proteins) has a role in enhancing beta-catenin (show CTNNB1 Proteins) signaling in acute myeloid leukemia (show BCL11A Proteins) harboring Fms-like tyrosine kinase-3 (show FLT3 Proteins) internal tandem duplication mutations
Review of the role of the most common form of FMS-like tyrosine kinase 3 (FLT3 (show FLT3 Proteins)) mutation (internal tandem duplication) in acute myeloid leukemia (show BCL11A Proteins).
the present cohort study demonstrated that FLT3 (show FLT3 Proteins)-ITD and DNMT3A (show DNMT3A Proteins) R882 double mutation predicts poor prognosis in Chinese AML (show RUNX1 Proteins) patients receiving chemotherapy or allo-HSCT treatment.
Although transient responses to FLT3 (show FLT3 Proteins) inhibitors are often observed in case of disease relapse, the most promising approach is the use of FLT3 (show FLT3 Proteins) inhibitors either in combination with induction chemotherapy or as consolidation/maintenance therapy after allogeneic hematopoietic cell transplantation.
The results indicate that DTX4 stable knockdown inhibits adipogenesis of 3T3-L1 cells through inhibiting C/EBPalpha (show CEBPA Proteins) and PPARgamma (show PPARG Proteins), arresting mitotic clonal expansion and regulating Wnt (show WNT2 Proteins) signaling pathway.
Functions as an ubiquitin ligase protein in vivo, mediating 'Lys48'-linked polyubiquitination and promoting degradation of TBK1, targeting to TBK1 requires interaction with NLRP4 (By similarity). Regulator of Notch signaling, a signaling pathway involved in cell-cell communications that regulates a broad spectrum of cell-fate determinations.
deltex 4 homolog
, E3 ubiquitin-protein ligase DTX4
, RING finger protein 155
, protein deltex-4
, deltex 4, E3 ubiquitin ligase
, deltex homolog 4
, LOW QUALITY PROTEIN: E3 ubiquitin-protein ligase DTX4