Jiajie Chen

Transplantation tolerance modifies donor-specific B cell fate to suppress de novo alloreactive B cells

Journal of Clinical Investigation · 2020 · 23 citations

The absence of alloantibodies is a feature of transplantation tolerance. Although the lack of T cell help has been evoked to explain this absence, herein we provide evidence for B cell-intrinsic tolerance mechanisms. Using a murine model of heart tolerance, we showed that alloreactive B cells were not deleted but rapidly lost their ability to differentiate into germinal center B cells and secrete donor-specific antibodies. We inferred that tolerant alloreactive B cells retained their ability to…

Data from ALKBH1 Drives Tumorigenesis and Drug Resistance via tRNA-decoding Reprogramming and Codon-biased Translation

2025-11-03 · 1 citations

<div>Abstract<p>Cancer cells utilize codon-biased translation to fuel tumorigenesis and drug resistance; however, underlying mechanisms remain poorly understood. In this study, we show that ALKBH1 is overexpressed in acute myeloid leukemia (AML) and essential for leukemia stem cell/leukemia-initiating cell self-renewal and AML development/maintenance but dispensable for normal hematopoiesis. ALKBH1 enhances mitochondrial assembly/function and oxidative phosphorylation, crucial for AM…

Supplementary Figures S1-S7 from ALKBH1 Drives Tumorigenesis and Drug Resistance via tRNA-decoding Reprogramming and Codon-biased Translation

2025-11-03

<p>Supplementary Figure S1. ALKBH1 is required for human AML cell survival/growth in vitro and human AML progression in vivo. Supplementary Figure S2. ALKBH1 is required for leukemic cell transformation, LSC/LIC self-renewal and AML maintenance. Supplementary Figure S3. ALKBH1 is dispensable for normal hematopoiesis. Supplementary Figure S4. ALKBH1 is required for mitochondrial functions in AML cells. Supplementary Figure S5. ALKBH1 specifically catalyzes the conversion of m5C/m5Cm to f5C…

Supplementary Tables S1-5 from METTL3-Mediated m<sup>6</sup>A Modification Controls Splicing Factor Abundance and Contributes to Aggressive CLL

2025-11-24

<p>Table S1 shows CLL sample information; Table S2 shows protein expression detected in CLL and normal B cells using TMT proteomics; Table S3 shows top 150 transcripts with highest m6A density in B cells; Table S4 shows sequences of shRNAs, sgRNAs, and primers used in our study; Table S5 shows cellular pathways enriched in our study.</p>

Supplementary Figures S1-8 from METTL3-Mediated m<sup>6</sup>A Modification Controls Splicing Factor Abundance and Contributes to Aggressive CLL

2025-11-24

<p>Fig S1. SF3B1 mutant CLL samples had pervasive changes in 3’ splice site. Fig S2. Omics analyses identify widespread post-transcriptional upregulation of splicing factors in CLL. Fig S3. Abundance of spliceosome complexes and RNA-binding proteins are associated with clinical outcomes in CLL. Fig S4. METTL3 is consistently upregulated along with differential m6A modification on transcripts of RNA splicing process in CLL. Fig S5. KO or pharmacological inhibition of METTL3 impacts cell gro…