Affinage

TAL1

T-cell acute lymphocytic leukemia protein 1 · UniProt P17542

Length
331 aa
Mass
34.3 kDa
Annotated
2026-06-10
100 papers in source corpus 50 papers cited in narrative 51 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TAL1 (SCL) is a class B bHLH transcription factor that orchestrates lineage-specific gene programs in hematopoiesis and the vascular endothelium by nucleating a multiprotein DNA-binding complex (PMID:8289805, PMID:9214632). It has no intrinsic homodimer or independent DNA-binding capacity and acts obligately through heterodimerization with class A bHLH E-proteins (E12/E47/HEB), the resulting heterodimers binding a defined subset of E-box elements (PMID:8289805, PMID:8159721). The LIM-only protein LMO2 (and LMO1) bridges the TAL1/E-protein heterodimer to LDB1 and GATA factors, assembling a higher-order complex that recognizes a bipartite E-box/GATA composite motif—an E-box ~7-9 bp upstream of a GATA site—across thousands of erythroid genomic loci, with TAL1 binding required prior to or simultaneous with GATA1 occupancy (PMID:9214632, PMID:10866689, PMID:17910069, PMID:26503782, PMID:20566737). The same complex operates in distinct cellular contexts: in erythroid cells GATA1 partners predominate, whereas in T-cells TAL1 binds alongside RUNX1 and ETS factors at lineage-specific sites, and TAL1 can also act as a DNA-binding-independent cofactor for GATA3 (PMID:21179004, PMID:9819382, PMID:20566737). Transcriptional output is switched by exchangeable coregulators—corepressors mSin3A/HDAC1, the LSD1/CoREST demethylase complex, and ETO2/MTGR1 dominate in undifferentiated cells and are progressively replaced by coactivators (p300, P/CAF, UTX, PADI4) during erythroid differentiation (PMID:10688671, PMID:19497860, PMID:19799863, PMID:10490830, PMID:11118214, PMID:26944678, PMID:24874575). TAL1 activity and stability are tuned by post-translational modifications: ERK/MAPK phosphorylation of Ser122 (driving hypoxia-induced degradation), PKA phosphorylation of Ser172 (disrupting LSD1 binding), AKT1 phosphorylation of Thr90 (promoting CHIP-mediated ubiquitination), Notch-induced Skp2/CHIP-dependent proteasomal turnover, and P/CAF acetylation that enhances DNA binding and releases mSin3A (PMID:8423803, PMID:11904294, PMID:22310283, PMID:19406989, PMID:17962192, PMID:11118214). In T-ALL, ectopic TAL1 establishes a self-reinforcing autoregulatory circuit with GATA3, RUNX1, and MYB and exerts oncogenic effect chiefly by sequestering and repressing E-protein tumor-suppressor activity, a mechanism that does not require TAL1 DNA binding (PMID:22897851, PMID:15193261, PMID:11439353, PMID:9507011); its aberrant expression depends on CTCF-mediated chromatin topology and long-range/interchromosomal enhancer-promoter interactions (PMID:23698277, PMID:32086528, PMID:24200685).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1994 High

    Established the foundational biochemical rule that TAL1 cannot bind DNA or function alone and must heterodimerize with class A bHLH E-proteins, defining its mechanism of DNA recognition.

    Evidence Binding-site selection, EMSA, two-hybrid and co-IP in Jurkat leukemic cells

    PMID:8159721 PMID:8289805

    Open questions at the time
    • Did not define how E-protein choice (E12/E47/HEB) shapes target gene selection
    • Did not resolve in vivo composite-motif binding
  2. 1994 Medium

    Resolved the dual transcriptional behavior of TAL1 by showing it can repress by sequestering E47 into less-active heterodimers yet activate in Id-rich settings, framing context-dependent output.

    Evidence Reporter assays with E-box promoters and EMSA; co-IP and CIP1 analysis in leukemic T cells

    PMID:8016094 PMID:9507011

    Open questions at the time
    • Mechanism of activation-domain incompatibility not structurally defined
    • Single-lab reporter-based interpretation
  3. 1997 High

    Defined LMO2 as the obligatory bridging molecule assembling a pentameric TAL1/E2A/GATA-1/LDB1 complex on a bipartite E-box/GATA motif, establishing the architecture of the erythroid regulatory complex.

    Evidence Co-IP, EMSA and in vivo assembly assays in erythroid cells; earlier reciprocal co-IP of LMO2-TAL1

    PMID:8078932 PMID:9214632

    Open questions at the time
    • Stoichiometry and affinity of the complex not quantified at this stage
    • Coregulator recruitment to the complex unaddressed
  4. 1996 High

    Provided in vivo genetic proof that the LMO2-TAL1 protein-protein interaction is required for synergistic oncogenic activity and that TAL1 overexpression alone drives clonal T-cell leukemia.

    Evidence Co-IP from double-transgenic mouse thymocytes and transgenic leukemia models, with CKII phosphorylation

    PMID:8605871 PMID:8895560

    Open questions at the time
    • Did not separate DNA-binding from protein-sequestration contributions to transformation
  5. 2004 High

    Demonstrated that TAL1 induces leukemia primarily by repressing E47/HEB tumor-suppressor activity rather than by activating downstream genes, and that this is independent of TAL1 DNA binding.

    Evidence ChIP of corepressor at the CD4 enhancer with E2A/HEB genetic epistasis and HDAC inhibitor pharmacology; DNA-binding-mutant transgenic mice

    PMID:11439353 PMID:15193261 PMID:9507011

    Open questions at the time
    • The full set of E-protein target genes mediating tumor suppression not enumerated
  6. 2000 High

    Identified the corepressor machinery (mSin3A/HDAC1) recruited via the TAL1 bHLH domain and showed its release during differentiation, defining the repressive state of the complex.

    Evidence Reciprocal co-IP, domain mapping, HDAC inhibitor and MEL differentiation assays

    PMID:10688671

    Open questions at the time
    • Did not establish the order of corepressor-to-coactivator exchange genome-wide
  7. 2000 High

    Established the activating arm of the switch by showing p300 binds the TAL1 bHLH domain and P/CAF acetylates a loop-region lysine to enhance DNA binding and displace mSin3A during erythroid differentiation.

    Evidence GST pulldown, co-IP, EMSA, in vitro/in vivo acetylation, dominant-negative P/CAF and MEL differentiation assays

    PMID:10490830 PMID:11118214

    Open questions at the time
    • Acetylation kinetics relative to other PTMs not mapped
    • Genome-wide acetylation-dependent targets not defined
  8. 2009 High

    Expanded the corepressor repertoire to LSD1/CoREST/HDAC and ETO2/MTGR1 complexes recruited through the TAL1 bHLH domain, linking TAL1 repression to histone H3K4 demethylation and erythroid silencing.

    Evidence Co-IP, mass spectrometry, domain mapping, ChIP at the p4.2/P4.2 promoter and shRNA knockdown with histone-mark analysis

    PMID:19497860 PMID:19799863

    Open questions at the time
    • How distinct corepressor modules are selected at individual loci unresolved
  9. 2012 High

    Connected signaling to chromatin output by showing PKA phosphorylation of Ser172 disrupts the TAL1-LSD1 interaction, triggering H3K4 hypermethylation and target activation.

    Evidence Co-IP, S172 mutagenesis, ChIP and PKA activator/inhibitor pharmacology

    PMID:22310283

    Open questions at the time
    • Upstream physiological PKA stimuli in erythropoiesis not defined
  10. 2002 High

    Defined ERK/MAPK phosphorylation of Ser122 as a degradation signal, showing growth-factor and hypoxia signaling control TAL1 protein turnover via the proteasome.

    Evidence Phosphopeptide mapping, S122 mutagenesis, ubiquitination and proteasome-inhibitor assays in endothelial cells; earlier ERK1/EGF kinase mapping

    PMID:11904294 PMID:8423803

    Open questions at the time
    • E3 ligase responsible for S122-dependent degradation not identified in these studies
  11. 2009 Medium

    Identified the AKT1-Thr90 / CHIP and Notch-Skp2/CHIP axes as ubiquitin-proteasome routes controlling TAL1 stability, with E47 heterodimerization protecting TAL1 from CHIP.

    Evidence Co-IP, ubiquitination assays, phosphorylation mapping and proteasome-inhibitor studies

    PMID:17962192 PMID:19406989

    Open questions at the time
    • Single-lab co-IP without reciprocal in vivo validation
    • Interplay between competing degradation pathways unquantified
  12. 2010 High

    Genome-wide ChIP-seq distinguished DNA-binding-dependent from DNA-binding-independent recruitment and revealed lineage-specific cofactor usage (GATA1 in erythroid; RUNX1/ETS1 in T-cells).

    Evidence ChIP-seq with motif analysis in primary erythroid cells and T-cell lines, plus co-IP of TAL1 with RUNX1/ETS1

    PMID:20566737 PMID:21179004

    Open questions at the time
    • Mechanism determining lineage-specific cofactor pairing not resolved
  13. 2015 High

    High-resolution ChIP-exo defined the precise positional architecture of TAL1 and GATA1 on a TG-N(7-8)-WGATAA composite motif, refining the structural logic of the erythroid complex.

    Evidence ChIP-exo and ChIP-seq with peak-resolution analysis across thousands of loci

    PMID:26503782

    Open questions at the time
    • Does not capture dynamics of complex assembly over differentiation
  14. 2012 High

    Mapped the T-ALL oncogenic circuit, showing TAL1 forms an autoregulatory loop with GATA3 and RUNX1 and feed-forward activation of MYB, with downstream targets like TRIB2 essential for leukemic survival.

    Evidence ChIP-seq, expression analysis and shRNA knockdown with survival assays

    PMID:22897851

    Open questions at the time
    • Hierarchy initiating the autoregulatory loop not established
  15. 2018 High

    Identified TAL1-complex target genes and cofactors driving leukemia maintenance (ARID5B superenhancer, NKX3.1) and a subtype-specific UTX/KDM6A dependency exploitable therapeutically.

    Evidence ChIP-seq, shRNA knockdown, rescue, zebrafish modeling and in vivo H3K27 demethylase inhibition

    PMID:20855495 PMID:26944678 PMID:29326336

    Open questions at the time
    • Generalizability of the UTX dependency across TAL1+ T-ALL subsets not fully delineated
  16. 2020 Medium

    Established that TAL1's own aberrant expression in T-ALL versus erythroid cells is governed by CTCF-mediated chromatin topology and long-range/interchromosomal enhancer-promoter loops.

    Evidence 3C/4C/Hi-C, ChIP, CRISPR deletion/inversion of a -31 kb CTCF boundary, and CTCF/hSET1/GATA1 knockdowns

    PMID:23698277 PMID:24200685 PMID:32086528

    Open questions at the time
    • Single-lab conformation studies; how topology selectively activates promoter-IV in T-ALL not mechanistically closed
  17. 2018 High

    Extended TAL1 function to lineage gatekeeping, showing SCL/TAL1 suppresses alternative (cardiac/paraxial) fates via Polycomb-PRC1 and ETO2-mediated repression in developmental contexts.

    Evidence Scl-null conditional knockout, ChIP-seq and genetic rescue with Eto2/Rybp knockdown; zebrafish endocardial cell-autonomy

    PMID:24075907 PMID:30560907

    Open questions at the time
    • Direct biochemical link between TAL1 and PRC1 recruitment not fully defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the cell integrates the multiple competing PTMs, degradation routes, cofactor exchanges, and chromatin-topology inputs into a single quantitative decision to activate versus repress a given TAL1 target remains unresolved.
  • No integrated model linking PTM state to coregulator selection genome-wide
  • No structure of the full higher-order complex on composite DNA
  • E3 ligase choice for each phospho-degron not unified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 7 GO:0003677 DNA binding 4 GO:0060090 molecular adaptor activity 4 GO:0042393 histone binding 1
Localization
GO:0005634 nucleus 2 GO:0005654 nucleoplasm 2
Pathway
R-HSA-1643685 Disease 5 R-HSA-4839726 Chromatin organization 5 R-HSA-74160 Gene expression (Transcription) 5 R-HSA-1266738 Developmental Biology 4
Partners
E2AGATA1GATA3LDB1LMO2LSD1P300RUNX1
Complex memberships
TAL1-ETO2/MTGR1 corepressor complexTAL1-LSD1/CoREST/HDAC1/HDAC2 corepressor complexTAL1/E2A/LMO2/LDB1/GATA-1 pentameric complexTAL1/LMO/LDB1/GATA3 T-cell complex

Evidence

Reading pass · 51 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 In erythroid cells, LMO2 (RBTN2) acts as an obligatory bridging molecule assembling a novel oligomeric DNA-binding complex comprising TAL1, E2A (E47), GATA-1, and LDB1/NLI. This pentameric complex binds a bipartite DNA motif consisting of an E-box (CAGGTG) followed ~9 bp downstream by a GATA site, and functions as a transcriptional transactivating complex. Co-immunoprecipitation, electrophoretic mobility shift assay (EMSA), in vivo assembly assays in erythroid cells The EMBO journal High 9214632
1994 TAL1 polypeptides do not have intrinsic DNA-binding activity and cannot form homodimers. Instead, TAL1 heterodimerizes with class A bHLH proteins (E12, E47, E2-2, HEB) to form heterodimers that bind DNA with preference for a subset of E-box elements represented by the consensus AACAGATGGT. Endogenous TAL1 heterodimers with DNA-binding activity were detected in Jurkat leukemic cell nuclear extracts. Binding-site selection assay, EMSA, nuclear extract analysis of Jurkat cells Molecular and cellular biology High 8289805
1994 TAL1 and E2A polypeptides form complexes in vivo in leukemic T cells (Jurkat). The bHLH domain of TAL1 selectively interacts with bHLH domains of E12 and E47 but not Id1. TAL1 does not self-associate to form homodimers, indicating that its in vivo functions depend on obligate heterologous interaction with E2A proteins. Two-hybrid assay and co-immunoprecipitation Proceedings of the National Academy of Sciences of the United States of America High 8159721
1994 The LIM protein RBTN2 (LMO2) is complexed with TAL1 phosphoprotein in the nucleus of erythroid cells. RBTN2 is not phosphorylated in this complex. A complex containing RBTN1 and TAL1 also occurs in a T-cell acute leukemia line. Co-immunoprecipitation with anti-RBTN2 and anti-TAL1 antisera, nuclear fractionation Proceedings of the National Academy of Sciences of the United States of America High 8078932
1994 TAL1 can both repress and activate transcription depending on cellular context. In cells permitting E47 homodimer formation, TAL1 represses transcription by sequestering E47 into TAL1-E47 heterodimers with lower transcriptional activity than E47-E47 homodimers. However, TAL1-E47 heterodimers are more resistant to negative regulation by Id proteins, allowing TAL1 to activate transcription in other settings. Transient transfection reporter assays with E-box-containing promoters, EMSA Proceedings of the National Academy of Sciences of the United States of America Medium 8016094
1993 TAL1 gene products (pp42TAL1 and pp22TAL1) are phosphoproteins containing phosphoserine residues. Serine residue 122 (S122) is a major phosphorylation site of pp42TAL1, phosphorylated in vivo by the extracellular signal-regulated protein kinase ERK1 in response to epidermal growth factor. Immunoprecipitation, phosphoamino acid analysis, in vitro kinase assay with ERK1, site-directed mutagenesis of S122, EGF stimulation Molecular and cellular biology High 8423803
1993 TAL1 protein products pp42TAL1 and pp22TAL1 are phosphorylated forms of the full-length and truncated TAL1 gene products, respectively. They are detectable by immunoprecipitation in T-ALL and erythroleukemia cell lines. Immunoprecipitation with anti-TAL1 antisera, phosphoamino acid analysis Oncogene Medium 8437851
1994 TAL1 N-terminal domain functions as a transcriptional activator of specific responsive reporter genes, providing evidence that chromosomal translocation-activated TAL1 can mediate transcriptional activation. Transient transfection reporter assay Proceedings of the National Academy of Sciences of the United States of America Medium 8058726
1996 LMO2 and TAL1 proteins form dimers in thymocytes of double-transgenic mice (not in single-transgenic mice). Dimer formation alters thymocyte development and potentiates T-cell tumorigenesis, providing formal proof that protein-protein interaction between LMO2 and TAL1 is required for their synergistic oncogenic activity. Co-immunoprecipitation from thymocytes of transgenic mice, transgenic mouse phenotypic analysis The EMBO journal High 8605871
1996 TAL1 is a serine phosphoprotein substrate for casein kinase II (CKII). Transgenic overexpression of tal1 alone causes clonal T-cell leukemia in mice. Co-expression with CKIIα dramatically accelerates leukemogenesis, likely indirectly through E protein heterodimeric partners of TAL1. Transgenic mouse model, in vitro phosphorylation assay The EMBO journal High 8895560
1998 TAL1 inhibits E47-mediated transcription because TAL1/E47 heterodimer activation domains are incompatible with each other. TAL1 inhibits E47 activity including E47-mediated activation of the CIP1 gene in leukemic T cells. The transforming properties of TAL1 result from its ability to inhibit E47 activity rather than from aberrant activation of downstream genes. Transient transfection reporter assays, co-immunoprecipitation, analysis in leukemic T-cell lines The Journal of biological chemistry Medium 9507011
1998 TAL1 and LMO proteins act as cofactors for GATA3 to activate RALDH2 transcription in T-ALL. TAL1, LMO, and GATA3 form a complex in vivo. A TAL1 mutant unable to bind DNA still activates RALDH2 transcription in the presence of LMO and GATA3, demonstrating DNA-binding-independent transcriptional activation by TAL1 as a GATA3 cofactor. Promoter analysis, transient transfection, co-immunoprecipitation, DNA-binding mutant analysis Molecular and cellular biology Medium 9819382
2000 The corepressor mSin3A is associated with TAL1 in murine erythroleukemia (MEL) and human T-ALL cells. The bHLH domain of TAL1 is both necessary and sufficient for TAL1-mSin3A interaction. TAL1 also interacts with HDAC1 in vitro and in vivo. HDAC inhibitor TSA relieves TAL1-mediated repression. TAL1 association with mSin3A and HDAC1 declines during DMSO-induced MEL cell differentiation, and constitutive mSin3A expression inhibits MEL differentiation. Co-immunoprecipitation, domain mapping, in vitro interaction assay, HDAC inhibitor treatment, reporter assay, MEL differentiation assay Molecular and cellular biology High 10688671
1999 p300 coactivator interacts directly with TAL1, co-immunoprecipitates with Tal1 in differentiating MEL cells, and is present with Tal1 in an E-box DNA-binding complex. The bHLH domain of Tal1 and N-terminal sequences of p300 are necessary for their interaction and for p300-stimulated transactivation. p300 augments TAL1-directed transcription from an E-box-containing promoter. Co-immunoprecipitation, GST pulldown, EMSA, reporter assay, deletion analysis Oncogene High 10490830
2000 TAL1 is acetylated in vivo and can be acetylated by p300 and P/CAF in vitro. P/CAF-mediated acetylation maps to a lysine-rich motif in the loop region, increases TAL1 DNA binding, and selectively inhibits TAL1 interaction with mSin3A corepressor. P/CAF and TAL1 acetylation increase during MEL cell differentiation. Acetylation-defective P/CAF mutant inhibits TAL1 acetylation, DNA-binding, and terminal erythroid differentiation. In vitro acetylation assay, in vivo acetylation detection, co-immunoprecipitation, EMSA, reporter assay, dominant-negative P/CAF mutant, MEL differentiation assay The EMBO journal High 11118214
2004 TAL1/SCL induces leukemia by repressing E47/HEB transcriptional activity. In tal1/scl thymocytes, the corepressor mSin3A is bound to the CD4 enhancer, whereas an E47/HEB/p300 activating complex is detected at the same site in wild-type thymocytes. Tal1/scl tumors are sensitive to HDAC inhibition. Genetic evidence: expression of tal1/scl in E2A or HEB heterozygous background accelerates disease. Chromatin immunoprecipitation, genetic epistasis (E2A/HEB heterozygous mice), HDAC inhibitor pharmacology, mouse model Cancer cell High 15193261
2001 The DNA-binding activity of TAL1 is not required to induce leukemia/lymphoma in mice; a DNA-binding mutant of TAL1 causes disease similar to wild-type TAL1. Both wild-type and DNA-binding mutant TAL1 form stable complexes with E2A proteins. TAL1 stimulates CD8+ and inhibits CD4+ thymocyte development in a manner similar to E2A-deficient mice, indicating that TAL1 contributes to leukemia by interfering with E2A function. Transgenic mouse model expressing DNA-binding mutant TAL1, co-immunoprecipitation, thymocyte phenotyping Oncogene High 11439353
2009 TAL1 is associated with histone demethylase complexes containing LSD1, CoREST, HDAC1, and HDAC2 in erythroleukemia and T-cell leukemia cells. The enzymatic domain of LSD1 represses TAL1-directed transcription. TAL1-associated LSD1 and HDAC1 are coordinately down-regulated during erythroid differentiation. TAL1 recruits LSD1 to the silenced p4.2 promoter in undifferentiated but not differentiated MEL cells. LSD1 knockdown derepresses TAL1 target genes with increased H3K4 dimethylation at their promoters. Co-immunoprecipitation, ChIP, shRNA knockdown, reporter assay, analysis of histone methylation marks Proceedings of the National Academy of Sciences of the United States of America High 19497860
2012 PKA-mediated phosphorylation of serine 172 (S172) of TAL1 specifically destabilizes the TAL1-LSD1 interaction, leading to H3K4 hypermethylation and activation of TAL1 target genes. Treatment with PKA activator forskolin derepresses target genes by reducing TAL1-LSD1 interaction, while PKA inhibitor H89 represses them. During erythroid differentiation, TAL1-associated LSD1 decreases while hSET1 recruitment increases at TAL1 targets. Co-immunoprecipitation, site-directed mutagenesis of S172, ChIP, PKA activator/inhibitor pharmacology, shRNA knockdown Oncogene High 22310283
2012 TAL1 forms a positive interconnected autoregulatory loop with GATA3 and RUNX1 in T-ALL cells. The TAL1 complex (with HEB, E2A, LMO1/2, GATA3, RUNX1) directly activates the MYB oncogene in a positive feed-forward loop. A critical downstream target, TRIB2, is oppositely regulated by TAL1 (activated) and E2A/HEB (repressed) and is essential for T-ALL cell survival. ChIP-sequencing, gene expression analysis, shRNA knockdown, functional survival assay Cancer cell High 22897851
2010 In erythroid cells, the majority of TAL1 genomic targets require its direct DNA-binding activity. However, one-fifth of TAL1 target sequences (mainly high-affinity sites) can recruit TAL1 independently of its DNA-binding activity. The preferred E-box motif for TAL1 in erythroid cells is CAGNTG. TAL1 binding is necessary prior to or simultaneous with GATA1 binding at co-occupied sites. ChIP-sequencing, gene expression analysis from primary fetal liver erythroid cells, motif analysis Genome research High 20566737
2010 TAL1 shows limited genomic binding overlap between erythroid and T-cell lineages. In T-cells, TAL1 preferentially binds ETS and RUNX motifs adjacent to E-boxes. TAL1 interacts with RUNX1 and ETS1, and these factors are critically required for TAL1 binding to T-cell differentiation-modulating genes. ChIP-sequencing, gene expression profiling, co-immunoprecipitation of TAL1 with RUNX1 and ETS1 The EMBO journal High 21179004
2007 Notch signaling accelerates TAL1/SCL protein degradation via ubiquitination and proteasomes. The Notch-induced degradation requires both Skp2 (SCF ubiquitin ligase substrate-binding subunit) and CHIP (chaperone-binding E3 ubiquitin ligase). The degradation sequence is located in the evolutionarily conserved C-terminus of TAL1. CHIP promotes TAL1 degradation using both its TPR domain and U-box ubiquitin ligase activity. Protein degradation assays, ubiquitination assays, co-immunoprecipitation, domain mapping, proteasome inhibitor studies The Journal of biological chemistry Medium 17962192
2009 TGF-β triggers polyubiquitylation and proteasomal degradation of TAL1. This effect is mediated by AKT1, which phosphorylates TAL1 at threonine 90, increasing TAL1 association with the E3 ubiquitin ligase CHIP. The E47 heterodimerization partner of TAL1 hinders the TAL1-CHIP association. Co-immunoprecipitation, ubiquitination assay, phosphorylation mapping, AKT1 kinase analysis, proteasome inhibitor studies Blood Medium 19406989
2002 Hypoxia stimulates phosphorylation of TAL1 at Ser122 by MAPK, followed by ubiquitination and proteasomal degradation in microvascular endothelial cells. Site-directed mutagenesis of S122 demonstrated that Ser122 phosphorylation is necessary for hypoxic acceleration of TAL1 turnover. Tryptic phosphopeptide mapping, chemical kinase inhibitors, site-directed mutagenesis of S122, ubiquitination assay, proteasome inhibitor, endothelial cell models The Journal of biological chemistry High 11904294
2009 Eto2/MTG16 and MTGR1 are heteromeric corepressors of TAL1 in murine erythroid progenitors. The interaction requires the bHLH domain of TAL1 and the TAF110 domain of Eto2. Mtgr1 and Eto2 enhance each other's association with TAL1. Eto2 occupies the P4.2 (protein 4.2) promoter in MEL cells and its occupancy decreases with differentiation. Eto2 and Mtgr1 augment Tal1-mediated gene repression. Tandem affinity purification / LC-MS/MS, co-immunoprecipitation, domain mapping, ChIP, reporter assay, MEL differentiation assay Biochemical and biophysical research communications High 19799863
2000 In human proerythroblasts and early erythroblasts, TAL1 forms a pentameric complex with E2A (E12), LMO2, LDB1, and retinoblastoma protein (pRb) that assembles on a consensus TAL1 binding site. pRb enhances the transcriptional activity of TAL1-E12-LMO2 and TAL1-E12-LMO2-LDB1 complexes. This pentameric complex negatively regulates c-kit promoter activity, with pRb potentiating the inhibitory effect. Co-immunoprecipitation, EMSA, reporter assay, transfection in TF1 and SAOS-2 cells Molecular and cellular biology Medium 10866689
2008 TAL1(bHLH) and E12(bHLH) preferentially form heterodimers rather than homodimers. LMO2 binds the TAL1/E12 heterodimer with high affinity (KA ~10^8 M^-1). The TAL1/E12/LMO2 complex forms in the presence or absence of DNA, but different complexes preferentially bind different E-box sequences. Biophysical methods (sedimentation equilibrium, circular dichroism), gel filtration, EMSA Proteins High 17910069
2014 TAL1 interacts with the peptidylarginine deiminase IV (PADI4). PADI4 acts as an epigenetic coactivator of TAL1 by counteracting repressive H3R2me2a histone marks placed by PRMT6 at the TAL1/PADI4 target gene IL6ST, augmenting H3K4me3 and increasing IL6ST expression. At the CTCF promoter, PADI4 acts as a repressor. Co-immunoprecipitation, ChIP, histone modification analysis, gene expression analysis Nature communications Medium 24874575
2016 UTX/KDM6A (H3K27 demethylase) is a coactivator of TAL1 and a major regulator of the TAL1 leukemic gene expression program. UTX functions as a pro-oncogenic cofactor essential for leukemia maintenance in TAL1-positive but not TAL1-negative T-ALL. This subtype-specific epigenetic dependency can be exploited therapeutically. Co-immunoprecipitation, shRNA knockdown, gene expression profiling, in vivo mouse xenograft with H3K27 demethylase inhibitor Genes & development High 26944678
2018 ARID5B is directly activated by the TAL1 complex via a superenhancer 135 kb upstream in T-ALL cells. ARID5B and TAL1 frequently co-occupy target genes and coordinately control their expression. ARID5B positively regulates expression of TAL1, its regulatory partners, and MYC. ARID5B is required for T-ALL cell survival, and forced ARID5B expression in zebrafish thymocytes causes tumor formation. ChIP-seq, shRNA knockdown, gene expression analysis, zebrafish model, enhancer analysis Genes & development High 29326336
2010 TAL1 directly activates NKX3.1 in T-ALL via a TAL1-LMO-LDB1 complex recruited by GATA-3 to the NKX3.1 promoter. TAL1-induced NKX3.1 activation is associated with loss of HP1-α binding and chromatin opening at the NKX3.1 promoter. NKX3.1 is required for T-ALL proliferation and partially rescues proliferation upon TAL1 knockdown. ChIP, shRNA knockdown, gene expression analysis, chromatin accessibility assay, rescue experiments The Journal of experimental medicine Medium 20855495
2011 TIF1γ (transcriptional intermediary factor 1γ) forms complexes with TAL1, occupies specific subsets of TAL1 DNA binding sites in vivo, and represses TAL1 transcriptional activity. Loss of TIF1γ results in deficient HSC transplantation activity and priming of ST-HSCs to myelomonocytic lineage. Co-immunoprecipitation, ChIP, conditional knockout mouse model, transplantation assay Cell stem cell Medium 21474105
2013 Oncogenic TAL1 expression in T-ALL is regulated by an interchromosomal interaction in which a T-cell-specific transcription factor c-Maf mediates a chromatin loop bringing the TAL1 promoter into proximity with a T-cell-specific regulatory element on chromosome 16. In erythroid cells, hSET1-mediated H3K4 methylation promotes a long-range intra-chromosomal loop bringing the +51 enhancer to TAL1 promoter 1; CTCF facilitates this interaction in erythroid but blocks it in T-ALL cells. Chromosome conformation capture (3C/4C), ChIP, CTCF knockdown, hSET1 knockdown Leukemia Medium 23698277
2013 In TAL1-expressing erythroid cells, the TAL1 locus adopts a chromatin looping 'hub' that brings all known TAL1 cis-regulatory elements including CTCF-bound insulators into close proximity. Loss of GATA1 results in hub disassembly and loss of CTCF/RAD21 from an insulator. TAL1/STIL gene looping patterns unique to T-ALL cells were identified at common TAL1/STIL breakpoint regions. Chromosome conformation capture (3C/4C), ChIP, GATA1 knockdown Blood Medium 24200685
2017 SF3B1 K700E mutant binds RBM15 more strongly than wild-type SF3B1. This altered SF3B1-RBM15 interaction promotes production of a novel short TAL1 splice variant (TAL1s) that contains the HLH DNA binding domain but lacks the N-terminal region. TAL1s loses its interaction with ETO2 corepressor, and TAL1s overexpression promotes erythroid differentiation and β-hemoglobin transcription. Co-immunoprecipitation, RNA splicing analysis, RT-PCR, overexpression and knockdown assays in K562 cells and CD34+ cord blood cells PloS one Medium 28545085
2011 TAL1 regulates cell cycle progression and proliferation in differentiating murine bone marrow monocyte precursors. TAL1 and its partner E47 bind E-box-GATA sequence elements in the Gata2 gene intron 4 and upstream of p16Ink4a by ChIP. Wild-type TAL1 but not a DNA-binding-defective mutant rescues the proliferative defect in Tal1-null monocyte/macrophage precursors, demonstrating requirement for direct DNA binding in this process. Conditional knockout, ChIP, DNA-binding mutant rescue experiment, cell cycle analysis Molecular and cellular biology High 20194619
2013 TAL1 regulates osteoclast differentiation by repressing DC-STAMP (a key regulator of osteoclast cell fusion). TAL1 directly targets the DC-STAMP gene and represses its expression by counteracting the activating functions of transcription factors PU.1 and MITF. ChIP, gene expression analysis (loss-of-function in osteoclast progenitors), reporter assay FASEB journal Medium 21990371
2015 KLF1 is required to stabilize GATA-1 and TAL1 occupancy at the β-globin locus and other erythroid genes. KLF1 knockdown reduces GATA-1 and TAL1 binding at the locus without affecting their expression, indicating KLF1 facilitates and/or stabilizes their chromatin association to generate active histone marks and chromatin looping. ChIP, shRNA knockdown of KLF1, histone acetylation analysis Biochimica et biophysica acta Medium 25528728
1995 Erythropoietin (Epo) elicits a rapid, dose-related increase in TAL1 mRNA by increasing gene transcription and stabilizing one mRNA species. Epo induces a TAL1 DNA-binding activity in erythroblast nuclear extracts, temporally associated with Epo-induced phosphorylation of nuclear TAL1 protein. Nuclear run-on transcription assay, EMSA, in vivo phosphorylation analysis in FVA cells The Journal of biological chemistry Medium 7744799
2015 GATA1 and TAL1 form a precisely organized complex at a compound bipartite motif consisting of a TG dinucleotide 7 or 8 bp upstream of a WGATAA motif across thousands of genomic locations in erythroid cells. Both factors generate characteristic ChIP-exo peaks around WGATAA motifs reflecting their positional arrangement within the complex. ChIP-exo (high-resolution ChIP with 5' exonuclease treatment and sequencing), ChIP-seq, MultiGPS peak analysis Molecular and cellular biology High 26503782
2018 SCL/TAL1 activates expression of co-repressor ETO2 and Polycomb-PRC1 subunits (RYBP, PCGF5) and maintains levels of H2AK119ub and H3K27me3. ETO2 and RYBP co-occupy most SCL target genes including cardiac/paraxial loci. Reduction of Eto2 or Rybp expression mimics the Scl-null cardiac phenotype, demonstrating that SCL suppresses alternative lineage fates through Polycomb-mediated repression. Conditional knockout (Scl-null), ChIP-seq, genetic rescue with Eto2/Rybp knockdown, single-cell gene expression analysis Nature communications High 30560907
2021 GATA2, TAL1, and ERG form an integrated subcircuit within a broader heptad of transcription factors that regulates the stem cell-to-erythroid transition in both healthy and leukemic cells. Chromatin accessibility at key heptad regulatory elements (bound by TAL1 among others) is predictive of cell identity. Manipulation of this triad can facilitate erythroid transition. Bulk and single-cell ChIP-seq, ATAC-seq, chromatin accessibility analysis, genetic perturbation Blood Medium 34075404
2020 A CTCF binding site at -31 kb (-31CBS) serves as a chromatin boundary defining the TAD and enhancer/promoter interaction required for TAL1 activation. In erythroid cells, deletion of -31CBS reduces chromatin accessibility and blocks the long-range interaction between the +51 enhancer and TAL1 promoter-1. In T-ALL cells, inversion of -31CBS disrupts the interaction between the +19 stem cell enhancer and leukemia-prone TAL1 promoter-IV, inhibiting TAL1 expression and leukemogenesis. CRISPR-mediated deletion/inversion, chromatin conformation assay (Hi-C/4C), ChIP, ATAC-seq Nucleic acids research Medium 32086528
2015 TAL1 directly represses DDiT4/REDD1 (an inhibitor of mTOR) in human hematopoietic stem/progenitor cells. ChIP experiments showed TAL1 binding at the DDiT4 promoter. TAL1 knockdown increases DDiT4 expression, reduces mTOR pathway activity, and impairs HSPC proliferation; TAL1 overexpression maintains hematopoietic potentials via mTOR pathway. ChIP, shRNA knockdown, conditional overexpression, mTOR pathway activity analysis (phospho-protein levels) Stem cells (Dayton, Ohio) Medium 25858676
2013 In zebrafish, tal1 plays a cell-autonomous role in regulating endocardial extension. tal1-deficient endocardial cells fail to generate a cohesive monolayer and show mislocalization of the tight junction protein ZO-1, indicating a defect in intercellular junction formation. The tal1-deficient endocardium also fails to maintain its identity, with endocardial cells ectopically initiating myocardial gene expression; however, junction defects precede identity loss. Blastomere transplantation (cell autonomy), live imaging, ZO-1 immunofluorescence, marker gene expression analysis in zebrafish tal1 mutants Developmental biology Medium 24075907
2009 Mef2C is a lineage-restricted direct target of Scl/Tal1 in megakaryocytic cells (but not erythroid cells). ChIP microarray analysis showed Scl directly binds Mef2C regulatory regions in megakaryocytic but not erythroid cells. Loss of Mef2C produces platelet defects similar to Scl-deficient mice, including reduced platelet count, increased platelet size, and impaired megakaryopoiesis in vitro. ChIP microarray (ChIP-chip), conditional knockout, platelet and megakaryocyte phenotyping Blood Medium 19211936
1993 TAL1 protein (pp42TAL1) is expressed in the nuclei of erythroid precursors and megakaryocytes in fetal liver and adult bone marrow, as well as in T-ALL cell lines. A punctate nuclear pattern suggests TAL1 may comprise part of a novel nuclear structure. TAL1 protein is also detectable in smooth muscle, some tissue macrophages, and endothelial cells of normal human tissues. Immunocytochemistry with anti-TAL1 monoclonal antibodies on human tissue sections and cell lines Blood Medium 7833471
1993 TAL1 is expressed in cultured human umbilical vein endothelial cells (HUVECs) at both RNA and protein levels. In situ hybridization revealed restricted TAL1 expression in endothelial cells of vessels within the white pulp and follicles of the spleen in vivo. Northern blot, immunoprecipitation, in situ hybridization Oncogene Medium 8414504
2010 In murine bone marrow monocyte precursors, TAL1 associates with E47 at E-box-GATA sequence elements in the Gata2 intron 4 and upstream of p16Ink4a. TAL1 knockout increases p16Ink4a mRNA and decreases Gata2 mRNA, and inhibits cell cycle progression and proliferation. ChIP, conditional Tal1 knockout, cell cycle analysis, gene expression analysis Molecular and cellular biology Medium 20194619
2005 Notch3 activation sustains aberrant TAL1 overexpression and phosphorylation in mature thymocytes. Phosphorylated TAL1 and Sp1 form an activator complex that occupies the cyclin D1 promoter in vivo specifically in the presence of pre-TCR signaling, establishing cyclin D1 as a downstream transcriptional target of the Tal1/Sp1 complex. ChIP (Tal1/Sp1 co-occupancy of cyclin D1 promoter), co-immunoprecipitation, Notch3 overexpression, reporter assay Blood Medium 16368887

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 The LIM-only protein Lmo2 is a bridging molecule assembling an erythroid, DNA-binding complex which includes the TAL1, E47, GATA-1 and Ldb1/NLI proteins. The EMBO journal 737 9214632
1999 Primers and protocols for standardized detection of minimal residual disease in acute lymphoblastic leukemia using immunoglobulin and T cell receptor gene rearrangements and TAL1 deletions as PCR targets: report of the BIOMED-1 CONCERTED ACTION: investigation of minimal residual disease in acute leukemia. Leukemia 291 10049045
2012 Core transcriptional regulatory circuit controlled by the TAL1 complex in human T cell acute lymphoblastic leukemia. Cancer cell 266 22897851
1989 Involvement of the TCL5 gene on human chromosome 1 in T-cell leukemia and melanoma. Proceedings of the National Academy of Sciences of the United States of America 249 2740341
1996 Tal-1 induces T cell acute lymphoblastic leukemia accelerated by casein kinase IIalpha. The EMBO journal 243 8895560
1993 Expression of tal-1 and GATA-binding proteins during human hematopoiesis. Blood 230 7678994
1994 The LIM protein RBTN2 and the basic helix-loop-helix protein TAL1 are present in a complex in erythroid cells. Proceedings of the National Academy of Sciences of the United States of America 205 8078932
2003 Combinatorial effects of Flk1 and Tal1 on vascular and hematopoietic development in the mouse. Genes & development 192 12569129
1996 Protein dimerization between Lmo2 (Rbtn2) and Tal1 alters thymocyte development and potentiates T cell tumorigenesis in transgenic mice. The EMBO journal 178 8605871
2004 TAL1/SCL induces leukemia by inhibiting the transcriptional activity of E47/HEB. Cancer cell 158 15193261
1994 Preferred sequences for DNA recognition by the TAL1 helix-loop-helix proteins. Molecular and cellular biology 155 8289805
2010 Genome-wide identification of TAL1's functional targets: insights into its mechanisms of action in primary erythroid cells. Genome research 151 20566737
1995 Xylose-metabolizing Saccharomyces cerevisiae strains overexpressing the TKL1 and TAL1 genes encoding the pentose phosphate pathway enzymes transketolase and transaldolase. Applied and environmental microbiology 151 8534086
1991 Two site-specific deletions and t(1;14) translocation restricted to human T-cell acute leukemias disrupt the 5' part of the tal-1 gene. Oncogene 145 1886719
2003 Lmo2 and Scl/Tal1 convert non-axial mesoderm into haemangioblasts which differentiate into endothelial cells in the absence of Gata1. Development (Cambridge, England) 142 14602685
2007 Early endocardial morphogenesis requires Scl/Tal1. PLoS genetics 134 17722983
1997 TAL1/SCL is expressed in endothelial progenitor cells/angioblasts and defines a dorsal-to-ventral gradient of vasculogenesis. Developmental biology 133 9405094
1993 Site-specific deletions involving the tal-1 and sil genes are restricted to cells of the T cell receptor alpha/beta lineage: T cell receptor delta gene deletion mechanism affects multiple genes. The Journal of experimental medicine 122 8459224
1995 Does activation of the TAL1 gene occur in a majority of patients with T-cell acute lymphoblastic leukemia? A pediatric oncology group study. Blood 121 7605997
1998 TAL1 and LIM-only proteins synergistically induce retinaldehyde dehydrogenase 2 expression in T-cell acute lymphoblastic leukemia by acting as cofactors for GATA3. Molecular and cellular biology 117 9819382
1994 Formation of in vivo complexes between the TAL1 and E2A polypeptides of leukemic T cells. Proceedings of the National Academy of Sciences of the United States of America 117 8159721
1993 TAL1, TAL2 and LYL1: a family of basic helix-loop-helix proteins implicated in T cell acute leukaemia. Seminars in cancer biology 117 8142619
2010 Differential genomic targeting of the transcription factor TAL1 in alternate haematopoietic lineages. The EMBO journal 111 21179004
1993 Clinical features and outcome of T-cell acute lymphoblastic leukemia in childhood with respect to alterations at the TAL1 locus: a Pediatric Oncology Group study. Blood 110 8471769
2017 SCL/TAL1: a multifaceted regulator from blood development to disease. Blood 108 28179281
2009 The transcriptional program controlled by the stem cell leukemia gene Scl/Tal1 during early embryonic hematopoietic development. Blood 108 19346495
2009 LSD1-mediated epigenetic modification is required for TAL1 function and hematopoiesis. Proceedings of the National Academy of Sciences of the United States of America 108 19497860
1995 Expression of TAL-1 proteins in human tissues. Blood 106 7833471
2016 UTX inhibition as selective epigenetic therapy against TAL1-driven T-cell acute lymphoblastic leukemia. Genes & development 99 26944678
1994 Transcriptional activation by TAL1 and FUS-CHOP proteins expressed in acute malignancies as a result of chromosomal abnormalities. Proceedings of the National Academy of Sciences of the United States of America 96 8058726
2005 Tie2Cre-mediated gene ablation defines the stem-cell leukemia gene (SCL/tal1)-dependent window during hematopoietic stem-cell development. Blood 93 15677556
1994 Positive and negative transcriptional control by the TAL1 helix-loop-helix protein. Proceedings of the National Academy of Sciences of the United States of America 87 8016094
2011 Notch1 inhibition targets the leukemia-initiating cells in a Tal1/Lmo2 mouse model of T-ALL. Blood 84 21670468
2000 mSin3A regulates murine erythroleukemia cell differentiation through association with the TAL1 (or SCL) transcription factor. Molecular and cellular biology 82 10688671
1997 Defects of the mismatch repair gene MSH2 are implicated in the development of murine and human lymphoblastic lymphomas and are associated with the aberrant expression of rhombotin-2 (Lmo-2) and Tal-1 (SCL). Blood 82 9116269
1996 T-cell-directed TAL-1 expression induces T-cell malignancies in transgenic mice. Cancer research 79 8912842
1993 Phosphorylation of the TAL1 oncoprotein by the extracellular-signal-regulated protein kinase ERK1. Molecular and cellular biology 79 8423803
2000 P/CAF-mediated acetylation regulates the function of the basic helix-loop-helix transcription factor TAL1/SCL. The EMBO journal 73 11118214
1999 p300 functions as a transcriptional coactivator for the TAL1/SCL oncoprotein. Oncogene 68 10490830
1993 Expression of the TAL1 proto-oncogene in cultured endothelial cells and blood vessels of the spleen. Oncogene 68 8414504
2009 Expression of the leukemia oncogene Lmo2 is controlled by an array of tissue-specific elements dispersed over 100 kb and bound by Tal1/Lmo2, Ets, and Gata factors. Blood 66 19171877
1995 Coordinate expression and developmental role of Id2 protein and TAL1/E2A heterodimer in erythroid progenitor differentiation. Blood 64 7540882
1993 Products of the TAL1 oncogene: basic helix-loop-helix proteins phosphorylated at serine residues. Oncogene 63 8437851
1998 The Tal1 oncoprotein inhibits E47-mediated transcription. Mechanism of inhibition. The Journal of biological chemistry 62 9507011
2012 Dynamic interaction between TAL1 oncoprotein and LSD1 regulates TAL1 function in hematopoiesis and leukemogenesis. Oncogene 61 22310283
2010 Gfi1 expression is controlled by five distinct regulatory regions spread over 100 kilobases, with Scl/Tal1, Gata2, PU.1, Erg, Meis1, and Runx1 acting as upstream regulators in early hematopoietic cells. Molecular and cellular biology 60 20516218
2010 NKX3.1 is a direct TAL1 target gene that mediates proliferation of TAL1-expressing human T cell acute lymphoblastic leukemia. The Journal of experimental medicine 58 20855495
2006 Transcriptional regulatory networks downstream of TAL1/SCL in T-cell acute lymphoblastic leukemia. Blood 58 16621969
2014 PADI4 acts as a coactivator of Tal1 by counteracting repressive histone arginine methylation. Nature communications 56 24874575
2012 SCL/TAL1 regulates hematopoietic specification from human embryonic stem cells. Molecular therapy : the journal of the American Society of Gene Therapy 56 22491213
1993 SIL-TAL1 deletion in T-cell acute lymphoblastic leukemia. Leukemia 56 8350619
2018 ARID5B as a critical downstream target of the TAL1 complex that activates the oncogenic transcriptional program and promotes T-cell leukemogenesis. Genes & development 55 29326336
1993 Clinical significance of TAL1 gene alteration in childhood T-cell acute lymphoblastic leukemia and lymphoma. Leukemia 54 8321044
2000 A pentamer transcriptional complex including tal-1 and retinoblastoma protein downmodulates c-kit expression in normal erythroblasts. Molecular and cellular biology 53 10866689
2018 MEIS1 Regulates Hemogenic Endothelial Generation, Megakaryopoiesis, and Thrombopoiesis in Human Pluripotent Stem Cells by Targeting TAL1 and FLI1. Stem cell reports 51 29358086
2016 SCL/TAL1 in Hematopoiesis and Cellular Reprogramming. Current topics in developmental biology 50 27137657
2006 Low SCL/TAL1 expression reveals its major role in adult hematopoietic myeloid progenitors and stem cells. Blood 50 16849639
2001 The DNA binding activity of TAL-1 is not required to induce leukemia/lymphoma in mice. Oncogene 50 11439353
2013 Aberrant TAL1 activation is mediated by an interchromosomal interaction in human T-cell acute lymphoblastic leukemia. Leukemia 49 23698277
2009 Mef2C is a lineage-restricted target of Scl/Tal1 and regulates megakaryopoiesis and B-cell homeostasis. Blood 49 19211936
2013 The role of Tal2 and Tal1 in the differentiation of midbrain GABAergic neuron precursors. Biology open 48 24167708
2013 Co-expression of TAL1 and ADH1 in recombinant xylose-fermenting Saccharomyces cerevisiae improves ethanol production from lignocellulosic hydrolysates in the presence of furfural. Journal of bioscience and bioengineering 47 23916856
1998 Enforced TAL-1 expression stimulates primitive, erythroid and megakaryocytic progenitors but blocks the granulopoietic differentiation program. Cancer research 45 9458106
2004 Characterization of DNA-binding-dependent and -independent functions of SCL/TAL1 during human erythropoiesis. Blood 41 14715640
2015 Genome-Wide Organization of GATA1 and TAL1 Determined at High Resolution. Molecular and cellular biology 39 26503782
2018 Identification of novel lncRNAs regulated by the TAL1 complex in T-cell acute lymphoblastic leukemia. Leukemia 38 29654272
2017 TAL1 as a master oncogenic transcription factor in T-cell acute lymphoblastic leukemia. Experimental hematology 37 28652130
2011 Adult hematopoiesis is regulated by TIF1γ, a repressor of TAL1 and PU.1 transcriptional activity. Cell stem cell 36 21474105
1995 Erythropoietin stimulates transcription of the TAL1/SCL gene and phosphorylation of its protein products. The Journal of biological chemistry 36 7744799
2018 The Role of TAL1 in Hematopoiesis and Leukemogenesis. Acta naturae 35 29713515
1997 The SCL/TAL1 gene: roles in normal and malignant haematopoiesis. BioEssays : news and reviews in molecular, cellular and developmental biology 35 9230693
2021 Disruption of a GATA2-TAL1-ERG regulatory circuit promotes erythroid transition in healthy and leukemic stem cells. Blood 34 34075404
2005 Cross talk among Notch3, pre-TCR, and Tal1 in T-cell development and leukemogenesis. Blood 34 16368887
1997 Simultaneous SIL-TAL1 RT-PCR detection of all tal(d) deletions and identification of novel tal(d) variants. British journal of haematology 34 9432040
2018 Tal1, Gata2a, and Gata3 Have Distinct Functions in the Development of V2b and Cerebrospinal Fluid-Contacting KA Spinal Neurons. Frontiers in neuroscience 33 29651232
2011 Tal1 regulates osteoclast differentiation through suppression of the master regulator of cell fusion DC-STAMP. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 33 21990371
2007 Ubiquitination and degradation of Tal1/SCL are induced by notch signaling and depend on Skp2 and CHIP. The Journal of biological chemistry 32 17962192
2018 SCL/TAL1 cooperates with Polycomb RYBP-PRC1 to suppress alternative lineages in blood-fated cells. Nature communications 31 30560907
2013 tal1 Regulates the formation of intercellular junctions and the maintenance of identity in the endocardium. Developmental biology 30 24075907
2010 A DNA-binding mutant of TAL1 cooperates with LMO2 to cause T cell leukemia in mice. Oncogene 30 21057528
2014 Synergistic effects of TAL1 over-expression and PHO13 deletion on the weak acid inhibition of xylose fermentation by industrial Saccharomyces cerevisiae strain. Biotechnology letters 29 24966040
2013 Chromatin looping defines expression of TAL1, its flanking genes, and regulation in T-ALL. Blood 29 24200685
2018 Oncogenic transcriptional program driven by TAL1 in T-cell acute lymphoblastic leukemia. International journal of hematology 28 30145780
2010 The TAL1/SCL transcription factor regulates cell cycle progression and proliferation in differentiating murine bone marrow monocyte precursors. Molecular and cellular biology 28 20194619
2002 Phosphorylation by mitogen-activated protein kinase mediates the hypoxia-induced turnover of the TAL1/SCL transcription factor in endothelial cells. The Journal of biological chemistry 28 11904294
2014 KLF1 stabilizes GATA-1 and TAL1 occupancy in the human β-globin locus. Biochimica et biophysica acta 27 25528728
2009 SIL-TAL1 fusion gene negative impact in T-cell acute lymphoblastic leukemia outcome. Leukemia & lymphoma 27 19562638
2018 The subclonal complexity of STIL-TAL1+ T-cell acute lymphoblastic leukaemia. Leukemia 26 29556024
2011 TAL1/SCL is downregulated upon histone deacetylase inhibition in T-cell acute lymphoblastic leukemia cells. Leukemia 26 21647153
2017 Splicing factor SF3B1K700E mutant dysregulates erythroid differentiation via aberrant alternative splicing of transcription factor TAL1. PloS one 25 28545085
2017 Defining the molecular basis of oncogenic cooperation between TAL1 expression and Pten deletion in T-ALL using a novel pro-T-cell model system. Leukemia 25 29151585
2009 TGF-beta induces degradation of TAL1/SCL by the ubiquitin-proteasome pathway through AKT-mediated phosphorylation. Blood 25 19406989
2016 microRNAs regulate TAL1 expression in T-cell acute lymphoblastic leukemia. Oncotarget 24 26882564
2009 Eto2/MTG16 and MTGR1 are heteromeric corepressors of the TAL1/SCL transcription factor in murine erythroid progenitors. Biochemical and biophysical research communications 24 19799863
2008 Assembly of the oncogenic DNA-binding complex LMO2-Ldb1-TAL1-E12. Proteins 24 17910069
1992 Frequency and DNA sequence of tal-1 rearrangement in children with T-cell acute lymphoblastic leukemia. Annals of hematology 24 1637887
2020 Alteration of CTCF-associated chromatin neighborhood inhibits TAL1-driven oncogenic transcription program and leukemogenesis. Nucleic acids research 23 32086528
2015 The SCL/TAL1 Transcription Factor Represses the Stress Protein DDiT4/REDD1 in Human Hematopoietic Stem/Progenitor Cells. Stem cells (Dayton, Ohio) 23 25858676
2012 GATA-binding protein 4 (GATA-4) and T-cell acute leukemia 1 (TAL1) regulate myogenic differentiation and erythropoietin response via cross-talk with Sirtuin1 (Sirt1). The Journal of biological chemistry 23 22773876
2006 p16Ink4a or p19Arf loss contributes to Tal1-induced leukemogenesis in mice. Oncogene 23 16407836

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