| 2008 |
E2-2/TCF4 is an essential and specific transcriptional regulator of plasmacytoid dendritic cell (pDC) development; constitutive or inducible deletion of E2-2 in mice blocked pDC development and abolished IFN response to unmethylated DNA. E2-2 directly activated multiple pDC-enriched genes including SpiB, Irf8, and Irf7. |
Conditional knockout mice, inducible deletion, direct target gene activation by ChIP/reporter assays, loss-of-function with defined cellular and molecular phenotype |
Cell |
High |
18854153
|
| 2010 |
Deletion of E2-2/TCF4 from mature peripheral pDCs caused their spontaneous differentiation into cells with classical dendritic cell (cDC) properties, including loss of pDC markers and acquisition of cDC signature genes. Genome-wide ChIP revealed direct binding of E2-2 to key pDC-specific, lymphoid, and certain cDC-enriched genes, indicating E2-2 actively maintains pDC cell fate by opposing the default cDC fate. |
Inducible deletion in mature pDCs, genome-wide chromatin immunoprecipitation (ChIP), gene expression profiling, flow cytometry |
Immunity |
High |
21145760
|
| 2016 |
TCF4 comprises two transcriptional isoforms, both required for optimal pDC development. The long TCF4 isoform is expressed specifically in pDCs; its deletion impaired pDC development and expanded non-canonical CD8+ cDCs. A conserved downstream enhancer is required for TCF4 upregulation during pDC differentiation, revealing a positive feedback loop. TCF4 expression and pDC differentiation were selectively sensitive to BET protein inhibition. |
Isoform-specific knockout mice, in vitro pDC differentiation, enhancer deletion, BET inhibitor treatment, gene expression profiling |
Immunity |
High |
27986456
|
| 2003 |
TCF4 is sumoylated at endogenous levels, with Lys297 identified as a sumoylation site. PIASy (SUMO E3 ligase) enhanced TCF4 sumoylation and beta-catenin-dependent transcriptional activity, while Axam (desumoylation enzyme) inhibited it. TCF4, SUMO-1, and PIASy co-localize in the nucleus within PML bodies. Mutation K297R reduced PIASy/beta-catenin-dependent activation, establishing that sumoylation of TCF4 is involved in beta-catenin-dependent gene expression in the Wnt pathway. |
Co-immunoprecipitation, sumoylation assays, PIASy overexpression, Axam siRNA knockdown, luciferase reporter, site-directed mutagenesis (K297R), co-localization |
The EMBO journal |
High |
12727872
|
| 1993 |
E2-2/TCF4 and E2A polypeptides are both present in B-cell-specific immunoglobulin enhancer E2-box binding complexes. In pre-B cells, complexes contain both E2-2 and E2A subunits; in mature B cells only E2A products are present, indicating differential developmental expression governs complex composition. |
Monoclonal antibody-based immunoprecipitation/supershift of E2-box binding complexes, Western blotting |
Molecular and cellular biology |
Medium |
8497267
|
| 1992 |
ITF2/E2-2 (TCF4) binds E-box sequences as homo-oligomers and forms hetero-oligomers with myogenin, E12, and HEB. Hetero-oligomerization with myogenin modulates DNA-binding specificity and binding off-rates. ITF2 can activate gene expression, establishing it as a functional E-protein class bHLH transcription factor. |
In vitro DNA binding assays, gel shift/EMSA, hetero-oligomerization assays, luciferase transcriptional activation |
Molecular and cellular biology |
Medium |
1312219
|
| 2009 |
MAD2B directly interacts with TCF4 (identified by yeast two-hybrid and confirmed by co-immunoprecipitation). The MAD2B–TCF4 interaction abolished the DNA-binding ability of TCF4 and blocked TCF4-mediated transcriptional activation (TOPFLASH assay). MAD2B knockdown in colorectal cancer cells led to epithelial-mesenchymal transdifferentiation by enhancing TCF4 binding to the Slug promoter and repressing E-cadherin expression. |
Yeast two-hybrid, co-immunoprecipitation, EMSA, TOPFLASH reporter, siRNA knockdown, chromatin immunoprecipitation, E-cadherin promoter reporter |
The Journal of biological chemistry |
High |
19443654
|
| 2006 |
Daxx was isolated as a TCF4-interacting protein by yeast two-hybrid and confirmed by co-immunoprecipitation. In the nucleus, Daxx reduced TCF4 DNA-binding activity and repressed TCF4 transcriptional activity, altering expression of downstream targets cyclin D1 and Hath-1 and inducing G1 phase arrest in colon cancer cells. |
Yeast two-hybrid, co-immunoprecipitation, EMSA, transcriptional reporter assays, flow cytometry cell cycle analysis |
The Journal of biological chemistry |
Medium |
16569639
|
| 2000 |
E2-2/TCF4 interacts with HASH-1 (human MASH-1) in both yeast and mammalian cells (confirmed by yeast two-hybrid and co-immunoprecipitation). The HASH-1/E2-2 complex binds an E-box (CACCTG) in vitro and transactivates an E-box-containing reporter in vivo, indicating E2-2 forms a functional bHLH heterodimer with the proneural factor HASH-1 in neuroblastoma cells. |
Yeast two-hybrid, co-immunoprecipitation in mammalian cells, EMSA, luciferase reporter assay |
Biochemical and biophysical research communications |
Medium |
10903890
|
| 2010 |
E2-2/TCF4 inhibits endothelial cell (EC) activation, migration, network formation, and proliferation, and suppresses in vivo angiogenesis (Matrigel plug assay). E2-2 interacts with Id1 via their HLH domains; Id1 interferes with E2-2-mediated transcriptional repression and rescues E2-2-mediated inhibition of angiogenesis. E2-2 inhibits VEGFR2 expression by suppressing VEGFR2 promoter activity. |
Adenoviral overexpression in vivo (Matrigel plug), EC migration/network/proliferation assays, mutational analysis of HLH domain, luciferase reporter (VEGFR2 promoter), siRNA knockdown |
Blood |
Medium |
20231428
|
| 2001 |
TCF4 is present in DNA complexes (with beta-catenin and E-cadherin) that bind the CAAAG Tcf recognition sequence in metastasis-inducing DNA fragments. Transfection of TCF4 expression vector inhibited osteopontin promoter activity stimulated by active Met-DNA fragments, indicating TCF4 acts as an endogenous repressor of osteopontin transcription by binding to CAAAG elements. |
Electrophoretic mobility shift assay (EMSA), Western blotting of DNA-protein complexes, co-transfection reporter assay, osteopontin mRNA measurement |
Cancer research |
Medium |
11454716
|
| 2001 |
ITF2/E2-2 suppresses melanogenic gene expression and Mitf transcription factor expression in melanocytes, as demonstrated by overexpression and antisense constructs with luciferase reporter assays and gene/protein expression analyses. Stable ITF2 overexpression reduced pigmentation and dendritic morphology; antisense knockdown enhanced both, establishing ITF2 as a functional repressor of the melanocyte differentiation program. |
Stable transfection of sense/antisense constructs, luciferase reporter assays with melanogenic gene promoters, gene expression analysis, pigmentation assays |
The Journal of biological chemistry |
Medium |
11382753
|
| 2008 |
TCF4 occupies 6,868 high-confidence chromatin binding sites genome-wide in the LS174T colorectal cancer cell line. TCF4-binding sites are predominantly distal from transcription start sites, are enriched for evolutionarily conserved A-C/G-A/T-T-C-A-A-A-G motifs, and frequently function as beta-catenin/TCF4-dependent enhancers in reporter assays. |
Chromatin immunoprecipitation combined with genome-wide DNA array (ChIP-chip), motif discovery, luciferase enhancer reporter assays |
Molecular and cellular biology |
High |
18268006
|
| 2008 |
Beta-catenin/TCF4 signaling directly upregulates the splicing factor SRp20 transcription. Activated beta-catenin increased endogenous SRp20 and stimulated an SRp20 promoter luciferase reporter, while dominant-negative TCF4 reduced both. Increased SRp20 was sufficient to alter alternative splicing of CD44 and a minigene reporter, demonstrating that the beta-catenin/TCF4 pathway regulates alternative splicing via SRp20. |
Dominant-negative TCF4 transfection, activated beta-catenin mutants, luciferase reporter assays, RT-PCR splicing assays, minigene reporter |
RNA |
Medium |
18952824
|
| 2012 |
Pitt-Hopkins syndrome-associated missense mutations in the bHLH domain of TCF4 alter subnuclear localization of the mutant protein and attenuate homo- and heterodimer formation (measured by HTRF). Mutations proximal to the bHLH domain do not alter localization or dimerization. TCF4 transactivates the NRXN1β and CNTNAP2 promoters in luciferase assays; PTHS mutants show variable, context-specific deficits in transactivating these promoters when co-expressed with different bHLH transcription factors. |
Homogenous time-resolved fluorescence (HTRF) dimerization assays, subnuclear localization imaging, luciferase reporter assays with NRXN1β and CNTNAP2 promoters |
Human mutation |
Medium |
22777675
|
| 2012 |
Kindlin 2 directly interacts with active beta-catenin and forms a tripartite complex with beta-catenin and TCF4 (confirmed by co-IP). Kindlin 2 selectively strengthens beta-catenin occupancy on the Axin2 promoter and enhances Axin2 gene expression, thereby promoting tumor cell invasion through a beta-catenin–Axin2–Snail cascade. |
Co-immunoprecipitation, chromatin immunoprecipitation (Axin2 promoter occupancy), reporter assays, invasion assays |
EMBO reports |
Medium |
22699938
|
| 2018 |
TRIB3 physically interacts with beta-catenin and TCF4 (confirmed by immunoprecipitation). TRIB3 overexpression increased recruitment of TCF4 and beta-catenin to promoters of Wnt target genes; TRIB3 knockdown decreased this recruitment. A peptide (P2-T3A6) that binds beta-catenin disrupted its interaction with TRIB3 and TCF4. |
Co-immunoprecipitation, chromatin immunoprecipitation, dual luciferase reporter, peptide inhibitor disruption assay, in vivo mouse models |
Gastroenterology |
Medium |
30365932
|
| 2017 |
TEAD4 associates with TCF4 to form a complex that co-binds target gene loci. VGLL4 targets this TEAD4-TCF4 complex to interfere with TEAD4-TCF4 functional interplay and suppress TCF4 transactivation, directly linking Wnt/beta-catenin and Hippo-YAP signaling at the transcription factor level. |
Co-immunoprecipitation, ChIP, reporter assays, VGLL4-mimicking peptide, in vivo mouse CRC model |
Nature communications |
Medium |
28051067
|
| 2014 |
ITF2/TCF4 prevents activation of the beta-catenin-TCF4 complex in colorectal cancer cells by competing with TCF4 for beta-catenin binding, thereby inhibiting expression of Wnt target genes. Stable ITF2 overexpression reduced proliferation and tumorigenic potential in xenograft models; ITF2 knockdown promoted xenograft tumor growth. |
Co-immunoprecipitation, TOPFLASH luciferase reporter, shRNA knockdown, stable transgenic overexpression, xenograft mouse models |
Gastroenterology |
Medium |
24846398
|
| 2015 |
TCF3 binds the MYC 3' Wnt-responsive element (WRE) to repress MYC expression. TCF3 depletion increases availability of the WRE for TCF4/beta-catenin complex binding. Inhibiting GSK3β causes an exchange of TCF3 for TCF4/beta-catenin at the MYC 3' WRE to activate MYC, and this TCF3-to-TCF4 switch controls MYC expression as quiescent cells re-enter the cell cycle. |
ChIP, shRNA-mediated TCF3 depletion, GSK3β inhibition, MYC expression analysis, cell cycle analysis |
Cell cycle |
Medium |
25659031
|
| 2019 |
The bHLH domain of TCF4 preferentially binds DNA containing 5-carboxylcytosine (5caC) at the flanking CpG of E-box elements. Crystal structures of TCF4 bHLH in complex with unmodified and 5caC-modified oligonucleotides reveal that the basic region adopts multiple conformations; Arg576 can interact with 5caC in the major groove. Five Arg residues in the basic region mutated in Pitt-Hopkins syndrome (including R569 and R576) are directly involved in 5caC recognition. |
Protein crystallography (crystal structures), in vitro DNA binding assays, mutagenesis of Pitt-Hopkins syndrome-associated residues |
Nucleic acids research |
High |
31081034
|
| 2016 |
TCF4 is a master regulator of the BPDCN oncogenic transcriptional program; its RNAi-mediated downregulation caused loss of the BPDCN-specific gene expression program and apoptosis. TCF4 controls BPDCN-specific super-enhancers, and BET inhibitors disrupt this TCF4-dependent transcriptional network, inducing apoptosis and retarding xenograft growth. |
RNAi screening, shRNA knockdown, gene expression profiling, BET inhibitor treatment, xenograft mouse models |
Cancer cell |
Medium |
27846392
|
| 2019 |
Gains of 18q21.2 targeting the TCF4 gene are the most frequent genetic alteration in ABC-like DLBCL. TCF4 overexpression in ABC-like DLBCL cell lines led to its occupancy on IGHM and MYC gene enhancers and increased expression of IgM and MYC at transcript and protein levels. Dominant-negative TCF4 constructs were synthetically lethal to cell lines harboring TCF4 copy gains. |
DNA copy number profiling, ChIP (TCF4 occupancy on IGHM and MYC enhancers), overexpression studies, dominant-negative constructs, BET PROTAC treatment, xenograft models |
Science translational medicine |
Medium |
31217338
|
| 2014 |
Zac1 directly activates the Tcf4 gene in neuronal progenitors by binding two cis-regulatory elements in the Tcf4 locus (shown by ChIP). Tcf4 upregulation enhances expression of the imprinted CDK inhibitor p57(Kip2), a Tcf4 target gene, and increases G1 phase cell number, establishing a Zac1→Tcf4→p57(Kip2) axis controlling cell cycle arrest in neuronal progenitors. |
ChIP identifying Zac1 binding at Tcf4 locus, luciferase reporter assays for cis-regulatory elements, Tcf4 overexpression, cell cycle analysis |
Molecular and cellular biology |
Medium |
24396065
|
| 2020 |
Tcf4 loss-of-function in mice causes mis-specification of cortical neurons, malformation of the corpus callosum and anterior commissure, hippocampal hypoplasia, and loss of GFAP-expressing midline glia. RNA-sequencing of E14.5 cortex shows Tcf4 functions as a transcriptional activator; its deletion downregulates genes linked to neurogenesis and neuronal maturation. |
Conditional knockout mice, immunohistochemistry, RNA-sequencing, morphological analysis |
Molecular and cellular neurosciences |
Medium |
32474139
|
| 2021 |
TCF4 and SOX11 biochemically interact (confirmed by co-IP) and cooperatively control commissure formation in vivo. scRNA-seq regulon analysis indicates TCF4 modulates activity of non-bHLH transcription factors (including FOXG1, SOX11, BRG1) in cortical projection neurons, and TCF4/SOX11 cooperatively regulate transcription of genes implicated in commissure formation. |
Single-cell RNA-sequencing, TF regulon analysis, co-immunoprecipitation, in vivo commissure formation assay |
Development |
Medium |
34184026
|
| 2009 |
TCF4 mutations in the basic domain of the bHLH domain impair heterodimerization with tissue-specific transcription factors less effectively than homodimerization in luciferase reporter assays, and the basic domain is a mutational hotspot in Pitt-Hopkins syndrome patients. |
Luciferase reporter assays, mutational analysis, patient cohort analysis |
Human mutation |
Medium |
19235238
|
| 2016 |
Tcf4 haploinsufficient mice show enhanced long-term potentiation in CA1 hippocampus. HDAC inhibitors normalized hippocampal LTP and memory recall in Tcf4+/- mice. Hdac2 isoform-selective knockdown was sufficient to rescue memory deficits, establishing that TCF4 haploinsufficiency acts partly through an HDAC2-dependent epigenetic mechanism to impair memory. |
Tcf4+/- mouse model, electrophysiology (LTP), behavioral assays, HDAC inhibitor treatment, antisense oligonucleotide Hdac2 knockdown, next-generation sequencing of hippocampal mRNA and methylated DNA |
Cell reports |
Medium |
27568567
|
| 2021 |
Acute cell-specific deletion of Tcf4 in adult excitatory neurons in vivo caused hyperexcitability and increased dendritic complexity, distinct from effects of embryonic deficiency. Transcriptomic analysis of adult-deleted neurons revealed Tcf4 targets in adult neurons are distinct from embryonic targets, with plasma membrane and ciliary genes specifically underlying adult neuron structure-function regulation. |
Adult conditional (Cre-lox) neuron-specific KO, electrophysiology, dendritic morphology analysis, FACS-sorted neuron transcriptomics |
Translational psychiatry |
Medium |
34564703
|
| 2022 |
Postnatal reinstatement of Tcf4 expression in neurons of a conditional Tcf4 mouse model of Pitt-Hopkins syndrome improved anxiety-like behavior, activity levels, innate behaviors, memory, partially corrected EEG abnormalities, and normalized expression of key TCF4-regulated genes, supporting that TCF4 haploinsufficiency is reversible postnatally by gene normalization. |
Conditional Tcf4 mouse model, viral gene therapy (postnatal Tcf4 reinstatement), behavioral assays, EEG recording, gene expression analysis |
eLife |
Medium |
35535852
|
| 2011 |
Connective tissue fibroblasts regulate muscle fiber type development and maturation via Tcf4-dependent signals; fibroblasts promote slow myogenesis by stimulating slow myosin heavy chain expression (Tcf4-dependent) and suppress fetal-to-adult muscle switching by repressing embryonic myosin (Tcf4-dependent). Low levels of Tcf4 intrinsically in myogenic cells also promote both slow and fast myogenesis, revealing a novel intrinsic mechanism. |
Tcf4GFPCre genetic manipulation of connective tissue fibroblasts, fiber type analysis, Tcf4 conditional KO, slow/fast myosin heavy chain expression analysis |
Development |
Medium |
21177349
|
| 2007 |
TCF4 expressed in the ventral diencephalon negatively regulates pituitary growth by restricting BMP and FGF signaling domains. TCF4-deficient mice show expanded Fgf10/Bmp4 expression domains rostrally, expanded Six6 in Rathke's pouch, and greatly enlarged anterior pituitary, indicating TCF4 restricts pituitary progenitor induction both extrinsically (via BMP/FGF) and intrinsically (via Six6). |
Tcf4 KO mice, in situ hybridization, immunohistochemistry of signaling molecule expression domains |
Developmental biology |
Medium |
17919533
|
| 2020 |
The intronic CTG18.1 trinucleotide repeat expansion in TCF4 causes formation of toxic CUG-containing nuclear RNA foci in corneal endothelial cells, sequesters splicing factors, and impairs splicing. Antisense oligonucleotides targeting the mutant CUG repeat RNA potently inhibited RNA foci in patient-derived cells and reversed pathological splicing changes in ex vivo human FECD corneas. |
Fluorescence in situ hybridization (FISH) for nuclear foci, splicing analysis, antisense oligonucleotide (ASO) treatment of patient cells and ex vivo corneas |
Human molecular genetics |
Medium |
29325021
|
| 2015 |
Expansion of the intronic CTG18.1 triplet repeat locus in TCF4 produces nuclear RNA foci containing expanded CUG transcripts in corneal endothelial samples from FECD patients with the expansion (foci in 33–88% of cells), but not in controls lacking the expansion, implicating toxic RNA as a mechanism in FECD pathogenesis. TCF4 constitutive exon expression was unaltered, suggesting haploinsufficiency is not the primary mechanism. |
Fluorescence in situ hybridization (FISH) for RNA foci, quantitative RT-PCR of TCF4 expression |
Investigative ophthalmology & visual science |
Medium |
25722209
|
| 2020 |
UHRF2 directly interacts with and sumoylates Tcf4 (confirmed by co-IP), stabilizing Tcf4 protein and sustaining hyperactive Wnt/beta-catenin signaling in intestinal tumors. Uhrf2-null ApcMin mice showed strongly reduced tumor initiation, and Uhrf2 loss suppressed Wnt/beta-catenin pathway activity, establishing a SUMOylation-dependent feedforward loop between Uhrf2 and Tcf4. |
Co-immunoprecipitation, sumoylation assays, conditional KO mice (Uhrf2 null on ApcMin background), organoid formation, Wnt reporter assays |
International journal of cancer |
Medium |
32372448
|
| 2009 |
HINT1 overexpression in hepatoma cells inhibits beta-catenin/TCF4 transcriptional activity and cyclin D1 expression. HINT1 co-immunoprecipitates with USF2, suggesting a physical interaction, while NFkappaB p65 nuclear translocation is also inhibited, establishing HINT1 as a repressor of the beta-catenin/TCF4 axis in hepatoma cells. |
Luciferase reporter assay (TCF4 reporter), co-immunoprecipitation, Western blot, nuclear fractionation |
International journal of cancer |
Low |
19089909
|
| 2006 |
E2-2/TCF4 is required for optimal expansion of pro-B cells; E2-2-deficient fetal liver cells showed reduced frequency of responding B cell progenitors at the pro-B stage. E2-2 deficiency also skewed peripheral B cell repertoire toward marginal zone (MZ) at the expense of follicular B cells, indicating E2-2 influences the follicular versus MZ B cell fate decision. |
Fetal liver cell transfer into irradiated Rag-deficient mice, stromal cell/IL-7 culture, real-time PCR of E-protein expression, flow cytometry of B cell subsets |
Journal of immunology |
Medium |
17082585
|
| 2008 |
E2-2/TCF4 is expressed during DN stages of thymocyte development and E2-2-null thymocytes display a partial block at the DN3 stage with reduced pre-Tα expression, a gene known to be regulated by E2A and HEB, indicating E2-2 operates cooperatively with E2A and HEB during early T cell development. |
E2-2 KO mouse analysis, flow cytometry of thymocyte populations, RT-PCR of E-protein and pre-Tα expression |
Molecular immunology |
Medium |
18384878
|
| 2019 |
Combined disruption of E2-2 and HEB in mice results in failure to express the early lymphoid program in common lymphoid precursors (CLPs) and near-complete block of B-cell development; ETPs were reduced and T-cell development perturbed. HSCs, erythro-myeloid progenitors, and innate immune cells were unaffected, demonstrating E2-2 and HEB are specifically required for lymphoid lineage specification. |
Double conditional KO mice (E2-2 and HEB), flow cytometry of progenitor and mature immune cell populations, adoptive transfer |
Frontiers in immunology |
Medium |
30936870
|
| 2019 |
TCF4 serves as a master regulator of the mesenchymal-like (MES) transcriptional program in melanoma, suppressing melanocytic and antigen presentation programs. Targeting TCF4 genetically or pharmacologically with a bromodomain inhibitor increased immunogenicity and sensitivity of MES cells to immune checkpoint blockade and targeted therapy. |
Single-cell multi-omics, genetic TCF4 knockdown, BRD inhibitor treatment, functional immunogenicity assays |
Cell |
Medium |
38181739
|
| 2011 |
TCF4 functions in macrophage lineage specification downstream of GM-CSF receptor signaling: forced expression of Tcf4 or stabilized beta-catenin is sufficient to promote macrophage differentiation in response to GM-CSF. GM-CSF regulates beta-catenin stability most likely via GSK3β, and GSK3β inhibition promotes macrophage over granulocyte colony formation from primary cells. |
Retroviral Tcf4 overexpression, stabilized beta-catenin expression, Wnt target gene reporter assays, GSK3β inhibition, primary colony assays |
Differentiation |
Medium |
22099176
|
| 2023 |
NF-κB p65 stabilizes ITF2/TCF4 protein by binding to its N-terminus and blocking Parkin-mediated ubiquitination of ITF2. Parkin acts as the E3 ubiquitin ligase for ITF2 ubiquitination. Intestinal epithelial-specific deletion of ITF2 enhanced nuclear p65 translocation and increased colitis-associated cancer tumorigenesis. |
Co-immunoprecipitation (p65–ITF2 interaction), ubiquitination assays, conditional intestinal epithelial KO, AOM/DSS cancer model, protein stability assays |
Nature communications |
High |
37185280
|
| 2018 |
CHAF1A directly interacts with TCF4 (confirmed by co-immunoprecipitation) and acts as a co-activator in the Wnt pathway. The CHAF1A-TCF4 complex binds promoter regions of c-MYC and CCND1, enhancing their expression and promoting gastric cancer cell proliferation. |
Co-immunoprecipitation, chromatin immunoprecipitation (ChIP at c-MYC and CCND1 promoters), overexpression and knockdown, luciferase reporter, in vivo xenograft |
EBioMedicine |
Medium |
30449701
|
| 2025 |
TCF4 controls the development of the DC2A (CD7+CD11blo) lineage of conventional dendritic cells in a TCF4-dependent manner from Siglec-H+CD115- pre-DC2 progenitors, as shown by conditional knockout and fate-mapping. |
Single-cell sequencing, conditional TCF4 knockout mice, fate-mapping, adoptive transfer |
Nature immunology |
Medium |
40702338
|