| 1999 |
Crystal structure (2.35 Å) of a ternary HoxB1-Pbx1-DNA complex revealed that the HoxB1 hexapeptide binds in a hydrophobic pocket in the Pbx1 homeodomain formed by a three-amino-acid insertion; Pbx1 contains an additional fourth alpha-helix C-terminal to the canonical homeodomain that contributes to hexapeptide binding and to stable Pbx1-DNA interaction. |
X-ray crystallography (2.35 Å resolution) |
Cell |
High |
10052460
|
| 1999 |
NMR studies showed that the fourth (C-terminal) alpha-helix of Pbx1 is unfolded in solution and folds only upon DNA binding; no conformational change was detected upon mixing Pbx1 with HoxB1 in the absence of DNA, suggesting DNA binding precedes or is required for stable Hox-Pbx1 complex assembly. |
Multidimensional NMR spectroscopy (1H, 15N, 13C) |
Journal of Molecular Biology |
High |
10448033
|
| 2003 |
Crystal structure (1.9 Å) of a HoxA9-Pbx1-DNA ternary complex revealed that the posterior Hox hexapeptide adopts an altered conformation compared to anterior Hox complexes, and that residues in the N-terminal arm of the Hox homeodomain determine DNA sequence specificity via indirect contacts, providing a structural basis for anterior-posterior Hox binding specificity modulated by Pbx1. |
X-ray crystallography (1.9 Å), DNA-binding assays with wild-type and mutant proteins |
Genes & Development |
High |
12923056
|
| 1995 |
The conserved pentapeptide motif (F/Y-P-W-M-R/K) located N-terminal to the Hox homeodomain is essential for cooperative DNA binding with Pbx1; point mutations at tryptophan and methionine abolished cooperativity; a wild-type pentapeptide peptide blocked cooperative binding and also stimulated Pbx1 DNA binding alone, establishing direct physical contact between the pentapeptide and Pbx1. |
In vitro DNA binding assays, point mutational analysis, competitive peptide inhibition |
Molecular and Cellular Biology |
High |
7565734
|
| 1995 |
Pbx1 (and E2A-Pbx1) binds DNA cooperatively with multiple Hox proteins (HoxA5, HoxB7, HoxB8, HoxC8, HoxD4) on the ATCAATCAA motif; cooperative binding required the homeodomain-dependent DNA-binding activity of both partners; in cotransfection assays HoxB8 suppressed E2A-Pbx1 transactivation. |
Electrophoretic mobility shift assay (EMSA), cotransfection/reporter assays |
Molecular and Cellular Biology |
High |
7791786
|
| 1996 |
The Pbx1 homeodomain is sufficient for cooperative DNA binding with pentapeptide-containing Hox proteins; a 25-residue predicted alpha-helix preceding the homeodomain inhibits Pbx1 DNA binding and Hox heterodimerization, and a sequence immediately C-terminal to the homeodomain (highly conserved, predicted alpha-helix) enhances monomeric DNA binding and cooperativity; heterodimerization places Pbx1 on the 5' TTGAT core and Hox on the adjacent 3' TGAT core. |
In vitro DNA binding assays with deletion and chimeric mutants |
Molecular and Cellular Biology |
High |
8657138
|
| 1997 |
Meis1 and pKnox1 dimerize with Pbx1 on a TGATTGAC motif; the Meis1/pKnox1-interaction domain in Pbx1 resides predominantly in a conserved N-terminal Pbx domain that is deleted in E2A-Pbx1, explaining why Meis1/pKnox1 fail to bind E2A-Pbx1; HPIP (a novel protein) also interacts with Pbx1 through the homeodomain and flanking sequences and inhibits PBX-HOX heterodimer DNA binding. |
EMSA, co-immunoprecipitation, yeast two-hybrid |
PNAS |
High |
9405651
|
| 2000 |
A novel protein HPIP (hematopoietic PBX-interacting protein) was identified by yeast two-hybrid as a Pbx1 interactor; HPIP is mainly cytosolic; it interacts with Pbx1 via the homeodomain and flanking sequences; HPIP inhibits PBX-HOX heterodimer DNA binding in EMSA and strongly inhibits E2A-PBX1 transactivation. |
Yeast two-hybrid, EMSA, transactivation reporter assays, subcellular fractionation |
Journal of Biological Chemistry |
Medium |
10825160
|
| 1999 |
An inhibitory 25-residue alpha-helix immediately N-terminal to the Pbx1 homeodomain binds the homeodomain and prevents DNA binding and Hox heterodimerization; an additional 39-residue region N-terminal to this helix mediates Pbx homodimerization and heterodimerization on DNA; Hox and Meis1/Prep1 partners relieve the inhibitory switch; the inhibitory switch is dispensable for myeloid immortalization by E2A-Pbx1. |
In vitro DNA binding assays, deletion mutagenesis, myeloid immortalization assays |
Oncogene |
Medium |
10637514
|
| 1997 |
Pbx1 heterodimers with different Hox proteins bind distinct DNA motifs; unique sequences in the N-terminal arm of the Hox homeodomain mediate this differential specificity; in vivo, Hox proteins directed E2A-Pbx1-mediated transactivation to cognate Hox-Pbx motifs, demonstrating Hox-dependent targeting of Pbx1 complexes to distinct genomic sites. |
EMSA with recombinant proteins, cotransfection/reporter assays, structural modeling |
Oncogene |
Medium |
9010234
|
| 1993 |
Expression of the E2A-PBX1 chimeric homeodomain protein under control of the immunoglobulin heavy chain enhancer in transgenic mice induced T-cell lymphomas and paradoxically increased both cell cycling and apoptosis in pretumorous lymphoid cells, establishing that the fusion oncogene simultaneously drives proliferation and programmed cell death in lymphoid cells in vivo. |
Transgenic mouse model, flow cytometry, histopathology |
Cell |
High |
8104101
|
| 2001 |
Pbx1-deficient mice die at E15/16 with widespread skeletal patterning defects restricted to Hox-dimerization-motif-bearing protein domains; in affected limbs and ribs, chondrocyte proliferation was markedly reduced with premature hypertrophy and precocious Col1a1 expression, establishing Pbx1 as a regulator of chondrocyte proliferation/differentiation timing without altering Hox gene expression. |
Pbx1 knockout mouse, histology, in situ hybridization, molecular marker analysis |
Development |
High |
11566859
|
| 2002 |
Pbx1-deficient embryos display pancreatic hypoplasia with severe defects in exocrine and endocrine cell differentiation; expression of Isl1 and Atoh5 was severely reduced; compound Pbx1+/−;Ipf1+/− mice develop overt diabetes, establishing in vivo genetic interaction between Pbx1 and Ipf1 (Pdx1) required for postnatal pancreatic function. |
Pbx1 knockout mouse, compound heterozygous mouse genetics (epistasis), molecular marker analysis, glucose tolerance testing |
Nature Genetics |
High |
11912494
|
| 2003 |
Pbx1-deficient mice completely lack adrenal glands; expression of steroidogenic factor-1 (SF-1) was reduced to minimal levels in Pbx1 mutant genital ridges, placing Pbx1 upstream of SF-1 in the adrenocortical development pathway; loss of Pbx1 also impaired Müllerian duct formation and mesonephric differentiation. |
Pbx1 knockout mouse, molecular marker analysis (SF-1 expression), histology |
Genesis |
High |
14595835
|
| 2003 |
In Pbx1-deficient kidneys, ureteric branching and elongation were reduced and nephron number was decreased; heterologous recombination explant cultures demonstrated that renal defects arose exclusively from mesenchymal (not ureteric) dysfunction, establishing Pbx1 as a regulator of mesenchymal-epithelial signaling during renal morphogenesis. |
Pbx1 knockout mouse, kidney explant heterologous recombination assays, molecular marker analysis |
Developmental Biology |
High |
12591246
|
| 2005 |
ChIP assays showed that Pbx1 binds the Hox11 promoter in spleen mesenchymal cells; Hox11 and Nkx2.5 expression are absent in Pbx1-null splenic anlage; Pbx1 and Hox11 genetically interact in spleen formation (double mutants have exacerbated phenotypes), establishing Pbx1 as a hierarchical upstream regulator in a Pbx1-Hox11 transcriptional pathway for spleen ontogeny. |
Pbx1/Hox11 double mutant mouse genetics, ChIP, in situ hybridization |
Development |
High |
15944191
|
| 2006 |
Pbx1/Pbx2 compound loss-of-function mice exhibit severe distal limb defects and Pbx1−/−;Pbx2−/− embryos lack limbs entirely; these defects are mediated by hierarchical control of Hox gene spatial distribution and Shh expression in the posterior limb/ZPA, demonstrating that Pbx1/Pbx2 act upstream of Hox genes and Shh to control limb axis patterning. |
Pbx1/Pbx2 double knockout mouse, in situ hybridization, molecular marker analysis |
Development |
High |
16672333
|
| 2008 |
Pbx1/Pbx2 compound loss-of-function establishes that axial skeletal patterning requires Pbx1/2 through genetic control of Polycomb and Hox expression in mesoderm and Pax1/Pax9 expression in sclerotome, placing Pbx1/2 in a hierarchical position above these axial patterning regulators. |
Pbx1/Pbx2 double knockout mouse, molecular marker analysis (Polycomb, Hox, Pax1/Pax9) |
Developmental Biology |
High |
18691704
|
| 2007 |
Using Rag1-deficient blastocyst complementation, Pbx1-null ES cells failed to generate common lymphoid progenitors (CLPs), resulting in complete absence of B and NK cells and partial impairment of T-cell development; restoration of Pbx1 expression rescued B-cell development from CLPs; conditional inactivation in pro-B (CD19+) cells showed Pbx1 is not required after CLP commitment, placing its essential function between HSC and CLP stages. |
Blastocyst complementation (Rag1-deficient), conditional gene rescue, adoptive transfer, flow cytometry |
Blood |
High |
17244677
|
| 2009 |
Pbx1 is a direct transcriptional target of Evi-1; Evi-1 overexpression upregulates Pbx1 transcription via the Pbx1 promoter; RNAi knockdown of Pbx1 inhibits Evi-1-induced bone marrow transformation but not transformation by E2A/HLF or AML1/ETO, establishing Pbx1 as specifically required downstream of Evi-1 in leukemogenesis. |
Promoter reporter assays, RNAi knockdown, bone marrow transformation assays, genetic epistasis |
Oncogene |
Medium |
19767769
|
| 2009 |
KLF4 and PBX1 are transcriptional activators of NANOG in human ESCs; PBX1 binds directly to a novel upstream enhancer and the proximal NANOG promoter (confirmed by ChIP and EMSA); knockdown or mutation of PBX1 binding sites reduces NANOG promoter activity; PBX1 cooperates synergistically with OCT4 and SOX2 to transactivate NANOG. |
ChIP, EMSA, luciferase reporter assay, RNAi knockdown, overexpression in hESCs |
Stem Cells |
Medium |
19522013
|
| 2010 |
Pbx1 negatively regulates Hoxa10-mediated osteoblast gene transcription; ChIP showed Pbx1 is associated with histone deacetylases (HDACs) at osteoblast-related gene promoters; loss of Pbx1 from promoters during differentiation correlates with increased histone acetylation, CBP/p300 recruitment, and decreased H3K9 methylation; Pbx1 acts through a Pbx-binding site that attenuates Hoxa10-mediated activation of osteocalcin and Bsp promoters. |
ChIP, shRNA knockdown, reporter assays with wild-type and mutant promoters, overexpression in mesenchymal cells |
Molecular and Cellular Biology |
Medium |
20439491
|
| 2011 |
PBX1 acts as a pioneer factor in breast cancer cells: ChIP-seq and FAIRE-seq showed PBX1 is loaded at specific genomic locations with open chromatin, promotes chromatin accessibility, reads specific epigenetic signatures, and guides ERα recruitment to a specific subset of genomic sites; PBX1 depletion abolishes estrogen-stimulated proliferation and controls >70% of the estrogen transcriptional response. |
ChIP-seq, FAIRE-seq, shRNA knockdown, expression profiling |
PLoS Genetics |
High |
22125492
|
| 2012 |
GCN5 (acetyltransferase subunit of the STAGA complex) directly interacts with the E2A portion of E2A-PBX1, acetylates E2A-PBX1, and increases its protein stability in cells; the E3 ubiquitin ligase HDM2 promotes E2A-PBX1 degradation; GCN5 inhibitor MB-3 decreases E2A-PBX1 acetylation and protein levels in leukemic cells. |
Co-immunoprecipitation, in vitro/cell-based acetylation assays, Western blot, pharmacological inhibition |
Leukemia |
Medium |
23044487
|
| 2012 |
Structural determination of the E2A PCET motif bound to the KIX domain of CBP/p300; residues throughout the helical PCET motif contact KIX; these residues are required for both KIX binding and bone marrow immortalization by E2A-PBX1, establishing the PCET/KIX interaction as mechanistically required for E2A-PBX1 leukemogenic activity. |
NMR/X-ray structural determination of peptide-KIX complex, mutagenesis, bone marrow immortalization assay |
Blood |
High |
22972988
|
| 2005 |
Pbx1 binds Hoxb1 autoregulatory enhancer elements (PH and PM sites); Prep1-Pbx1 forms ternary complexes with Hoxb1 at the R3/PM2 combination sufficient to drive hindbrain r4 reporter expression in vivo; a high-affinity PM site (R2/PM3) inhibits ternary complex formation and restricts reporter expression, demonstrating that multiple Prep1-Pbx1 and Pbx1-Hox binding sites cooperate to modulate Hoxb1 autoregulation. |
In vitro binding assays, transgenic reporter analysis in chick and mouse embryos, mutagenesis of binding sites |
Molecular and Cellular Biology |
Medium |
16166636
|
| 2008 |
Pbx1 is a direct transcriptional target of Notch3; the Notch3/CSL protein complex binds directly to the CSL-binding sequence in the Pbx1 promoter; ectopic Pbx1 expression partially reverses the growth-inhibitory effect of gamma-secretase inhibitor; Pbx1 shRNA knockdown reduces cell proliferation and tumorigenicity in ovarian cancer cells. |
ChIP (Notch3/CSL-Pbx1 promoter), reporter assay, shRNA knockdown, rescue experiment with ectopic expression |
Cancer Research |
Medium |
18974129
|
| 2014 |
Prep1 and Meis1 competitively heterodimerize with Pbx1; Prep1 posttranslationally reduces Meis1 stability by sequestering Pbx1 from Meis1; loss of Prep1 allows Meis1 to remain bound to Pbx1 and remain stable, enabling oncogenic transformation; Pbx1 can therefore function as either oncogene or tumor suppressor depending on which partner (Meis1 vs. Prep1) it dimerizes with. |
Co-immunoprecipitation, protein stability assays, transformation assays in mouse embryonic fibroblasts, overexpression/knockdown |
PNAS |
Medium |
24578510
|
| 2016 |
PBX1 directly represses Onecut2 (to inhibit lateral fates) and directly activates Pitx3 (to promote mDAn development) and Nfe2l1 (to protect from oxidative stress) in midbrain dopaminergic neurons; PBX1 and NFE2L1 levels are severely reduced in dopaminergic neurons of the substantia nigra in Parkinson's disease patients. |
ChIP, conditional knockout mouse (loss of function), gene expression analysis, human PD tissue analysis |
The EMBO Journal |
Medium |
27354364
|
| 2016 |
PBX1 directly binds the STAT3 promoter and positively regulates STAT3 transcription in ovarian cancer; silencing PBX1 in platinum-resistant cells reduces stem-like properties and sensitizes cells to carboplatin; a STAT3/JAK2 inhibitor potently sensitizes platinum-resistant cells to carboplatin in vivo. |
ChIP, shRNA knockdown, overexpression, in vivo xenograft model |
Cancer Research |
Medium |
27590741
|
| 2016 |
Pbx1-d (dominant-negative isoform lacking DNA-binding and Hox-binding domains) expression in CD4+ T cells expands follicular helper T cells (TFH) and impairs Foxp3+ Treg homeostasis; Pbx1-d-Tg CD4+ T cells upregulate miR-10a, miR-21, and miR-155; Pbx1-d directly regulates CD44 expression through two promoter binding sites, with enhanced MEIS co-factor recruitment relative to normal Pbx1-b. |
Transgenic mouse model, flow cytometry, ChIP, reporter assay, co-factor recruitment assay |
Journal of Immunology / Molecular Immunology |
Medium |
27296664 28257976
|
| 2016 |
Pbx1 restrains myeloid maturation and maintains lymphoid potential in multipotent progenitors; conditional Pbx1 knockout reduces MPP and CMP pools due to aberrantly rapid myeloid differentiation, associated with premature myeloid gene expression and reduced Meis1 expression (a Pbx1 dimerization partner), placing Pbx1 upstream of Meis1-dependent transcriptional programs in hematopoietic progenitor lineage specification. |
Conditional Pbx1 knockout mouse, flow cytometry of purified progenitors, transcriptional profiling, proliferation/differentiation assays |
Journal of Cell Science |
Medium |
23660001
|
| 2016 |
Pbx1 is required for adult subventricular zone (SVZ) neurogenesis; retroviral Cre-mediated deletion in Pbx2-deficient SVZ stem/progenitor cells significantly reduced neuron production and increased oligodendrocyte generation; loss of Pbx1 in neuroblasts compromised cell survival; ChIP from endogenous tissues detected PBX1 binding to regulatory regions of Dcx and Th weeks before their expression, suggesting a priming/pioneer role. |
Retroviral Cre delivery in conditional/Pbx2-null mice, neurosphere assays, ChIP from endogenous brain tissue |
Development |
Medium |
27226325
|
| 2018 |
SETDB2 is directly transcriptionally activated by E2A-PBX1 in pre-BCR+ ALL and suppresses expression of cell-cycle inhibitor CDKN2C through histone H3K9 tri-methylation, establishing an oncogenic pathway subordinate to E2A-PBX1 that silences a tumor suppressor. |
ChIP, shRNA knockdown, H3K9me3 ChIP, in vitro/in vivo leukemia maintenance assays |
Cell Reports |
Medium |
29694893
|
| 2019 |
USP9x deubiquitinase interacts with PBX1 and stabilizes PBX1 protein by attenuating Lys48-linked polyubiquitination; USP9x inhibitor WP1130 induces PBX1 degradation and promotes prostate cancer cell apoptosis, identifying USP9x as a specific deubiquitinase for PBX1. |
Co-immunoprecipitation, ubiquitination assays, pharmacological inhibition (WP1130), siRNA knockdown, apoptosis assays |
Journal of Biological Chemistry |
Medium |
30718275
|
| 2019 |
PBX1 promotes NK cell development by directly binding the Nfil3 promoter and upregulating NFIL3/E4BP4 transcription; conditional PBX1 knockout in hematopoietic cells reduces pre-NKP and rNKP progenitors similarly to NFIL3 deficiency; CRISPR knockout of the PBX1-binding site in the Nfil3 promoter in vivo reduces NK precursor and mature NK cells; asparagine N286 in the PBX1 homeodomain is required for Nfil3 promoter binding. |
Conditional knockout mouse, CRISPR-mediated binding-site deletion in vivo, ChIP, site-directed mutagenesis |
FASEB Journal |
High |
32190943
|
| 2019 |
PBX1 expression in decidual NK (dNK) cells is upregulated through AKT1 pathway activation downstream of MHC-G/ILT2 receptor interaction; PBX1 drives pleiotrophin and osteoglycin transcription in dNK cells to promote fetal development; Pbx1 inactivation in mouse dNK cells impairs fetal development by reducing growth-promoting factors from CD49a+PBX1+ dNK cells. |
Conditional knockout mouse (dNK-specific), pathway inhibition, ChIP/transcriptional assays, human patient samples |
Science Translational Medicine |
Medium |
32238574
|
| 2020 |
E2A-PBX1 preferentially binds genomic loci co-occupied by RUNX1 and gene-activating machinery (p300, MED1, H3K27ac); E2A-PBX1 directly interacts with RUNX1 through the PBX1 homeodomain region; E2A-PBX1 chromatin binding at enhancers depends on the RUNX1 interaction but not on PBX1 homeodomain DNA-binding activity; RUNX1 is required for E2A-PBX1 target gene activation and leukemogenesis; E2A-PBX1 also directly activates the RUNX1 locus itself. |
ChIP-seq, co-immunoprecipitation, CRISPR/mutagenesis, transcriptome analysis, cell transformation assays |
Blood |
High |
32276273
|
| 2021 |
Mediator subunit MED1 directly interacts with the E2A activation domain of E2A-PBX1; MED1 depletion by CRISPR/Cas9 specifically impairs E2A-PBX1-dependent gene activation and leukemic cell growth; DNA-bound RUNX1 recruits E2A-PBX1 to target loci and EBF1 further stabilizes this interaction, establishing a multi-factor complex required for E2A-PBX1 oncogenic transcription. |
Co-immunoprecipitation, CRISPR/Cas9 knockout, ChIP-seq, transcriptome analysis, in vitro binding assays |
PNAS |
High |
33542097
|
| 2003 |
Glucocorticoid receptor (GR) physically interacts with Pbx1 in vivo (co-immunoprecipitation); the GR DNA-binding domain is required for GC/RA synergy; GC potentiates RA-induced Hoxb-1 expression through the Pbx1/HOXB1-bound autoregulatory element b1-ARE without requiring GR binding to that element, suggesting GR-Pbx1 cross-talk regulates Hox target gene expression. |
Co-immunoprecipitation, reporter assays, domain-deletion analysis |
Biochemical Journal |
Medium |
12487626
|
| 2007 |
A novel zinc-finger protein ZFPIP physically binds PBX1 in vivo and prevents the binding of HOXA9/PBX1 complexes to their consensus DNA site, identifying a new class of PBX1 inhibitory partner that modulates Hox-PBX1 DNA binding. |
Yeast two-hybrid, co-immunoprecipitation, EMSA |
Mechanisms of Development |
Medium |
17353115
|
| 2019 |
A de novo missense mutation p.Arg235Gln in the TALE homeodomain nuclear localization signal of PBX1 impairs nuclear localization of the protein and abolishes its physical interaction with CBX2 and EMX2 (proteins required for testis-determination), providing a mechanism for 46,XY gonadal dysgenesis caused by this mutation. |
Subcellular localization assay, co-immunoprecipitation, patient mutation analysis |
Human Mutation |
Medium |
31058389
|
| 2022 |
METTL3-mediated m6A modification stabilizes PBX1 mRNA; PBX1 acts as a transcription factor inducing GCH1 expression (confirmed by ChIP); the METTL3-PBX1-GCH1 axis increases tetrahydrobiopterin (BH4) levels in gastric cancer cells to promote tumor progression. |
m6A RIP-seq, ChIP, Western blot, xenograft model, ELISA/LC-MS |
Cancer Communications |
Medium |
35261206
|
| 2022 |
PBX1 is ectopically expressed in chr1q-amplified multiple myeloma via amplification and epigenetic activation of its 3D regulatory domain; PBX1 binds to reprogrammed superenhancers and directly regulates a FOXM1-dependent transcriptional program; pharmacological disruption with T417 (a novel PBX1 small molecule inhibitor docking to the PBX1-DNA interface) is selectively toxic to chr1q-amp myeloma and solid tumor cells. |
Multi-omics (ChIP-seq, 3D chromatin), pharmacological inhibition (T417/thiostrepton), patient genomic data integration |
Blood |
Medium |
35015835
|
| 2023 |
Pbx1 directly regulates B-cell homeostasis by targeting proliferation and apoptosis pathway genes; B cell-specific Pbx1 knockout in mice causes excessive humoral responses and enhanced germinal center reactions; ChIP and CUT&TAG assays identified direct Pbx1 target genes controlling B-cell survival and proliferation; enforced PBX1 expression in SLE patient B cells attenuates their survival and proliferative capacity. |
B cell-specific conditional knockout mouse, ChIP, CUT&TAG, RNA-seq, overexpression in human SLE B cells |
Arthritis & Rheumatology |
Medium |
36862399
|
| 2023 |
PBX1/2 and HAND2 cooperate to direct a limb-specific gene regulatory network (GRN) in posterior hindlimb mesenchymal cells; tissue-specific and temporally controlled mutagenesis combined with genome-wide PBX1 binding profiling across multiple embryonic tissues shows that HAND2 interacts with subsets of PBX1-bound regions to restrict PBX1 activity to limb-specific GRNs, explaining how ubiquitous PBX1 achieves tissue-specific functions. |
Conditional/temporal knockout mouse, multi-omics (ChIP-seq across tissues, ATAC-seq), co-immunoprecipitation/interaction assays |
Nature Communications |
High |
37414772
|
| 2023 |
TRIM26 E3 ubiquitin ligase binds PBX1 (identified by affinity purification-MS) and mediates K48-linked polyubiquitination and proteasomal degradation of PBX1 in a RING domain-dependent manner; TRIM26 inhibits PBX1 transcriptional activity and downregulates PBX1 target gene RNF6. |
Affinity purification-MS, co-immunoprecipitation, ubiquitination assay, domain deletion (RING), reporter assay, xenograft model |
International Journal of Biological Sciences |
Medium |
37324936
|
| 1996 |
An internal domain of Pbx1 (upstream of the homeodomain, highly conserved among Pbx proteins) selectively represses transcription induced by the Sp1 activation domain but not VP16 or p53, and this repression activity does not require homeodomain-dependent DNA binding, indicating Pbx1 can regulate transcription through DNA-binding-independent mechanisms. |
Transient transfection reporter assays, domain-deletion analysis |
PNAS |
Medium |
8552663
|
| 2021 |
PBX1 is required for MPN progression driven by JAK2V617F; in compound JAK2V617F × Pbx1-null mice (JP model), typical MPN features (thrombocythemia, granulocytosis, splenomegaly, cytokine-independent growth) are absent; PBX1 controls part of the molecular pathways deregulated by JAK2V617F, placing PBX1 as a required co-effector downstream or parallel to JAK2V617F signaling in MPN. |
Conditional double-mutant mouse model (JAK2V617F × Pbx1 knockout), flow cytometry, transcriptome profiling |
Stem Cell Reports |
Medium |
34678207
|