Hang Nguyen
A5032263171- Glycosylation and Glycoproteins Research
- Monoclonal and Polyclonal Antibodies Research
- CAR-T cell therapy research
- CRISPR and Genetic Engineering
- Ubiquitin and proteasome pathways
- Lymphoma Diagnosis and Treatment
- Immune Cell Function and Interaction
- Immunotherapy and Immune Responses
- Biochemical and Molecular Research
Ludwig-Maximilians-Universität München
2025
National Institutes of Health
2023
National Cancer Institute
2023
Abstract Diffuse large B-cell lymphoma (DLBCL) can be subdivided into the activated (ABC) and germinal center B cell–like (GCB) subtypes. Self-antigen engagement of receptors (BCR) in ABC tumors induces their clustering, thereby initiating chronic active signaling activation NF-κB PI3 kinase. Constitutive BCR is essential some GCB but primarily activates We devised genome-wide CRISPR–Cas9 screens to identify regulators IRF4, a direct transcriptional target an indicator proximal DLBCL....
<title>Abstract</title> Co-translational N-terminal modifications such as methionine excision, acetylation, and myristoylation contribute to protein stability, localization, folding (1). Disrupting these exposes short degron motifs that trigger degradation via the ubiquitin-proteasome system, safeguarding proteome (2). While acetylation typically protects proteins, it may also promote through Ac/N-degron pathway (3). Src family kinases (SFKs), key regulators of signaling tumorigenesis,...
<p>Supplemental Figure 1. IRF4-GFP knock-in reporter cell lines. Supplemental 2. CRISPR screen in adult T-cell lymphoma and controls. 3. The OST is essential for DLBCL. 4. role of the complex radiation chimeras. 5. B-cell receptor glycosylated by complex. 6. deglycosylation leads to higher surface expression. 7. signaling changes proximal BCR components. 8. recruitment CD22 on alterations GCB 9. internalization My-T-BCR formation glycosylation deficient cells. 10. NGI-1 synergizes with...
<p>Supplemental Figure 1. IRF4-GFP knock-in reporter cell lines. Supplemental 2. CRISPR screen in adult T-cell lymphoma and controls. 3. The OST is essential for DLBCL. 4. role of the complex radiation chimeras. 5. B-cell receptor glycosylated by complex. 6. deglycosylation leads to higher surface expression. 7. signaling changes proximal BCR components. 8. recruitment CD22 on alterations GCB 9. internalization My-T-BCR formation glycosylation deficient cells. 10. NGI-1 synergizes with...
<div>Abstract<p>Diffuse large B-cell lymphoma (DLBCL) can be subdivided into activated like (ABC) and germinal center B-cell-like (GCB) DLCBL. Self-antigen engagement of receptors (BCRs) in ABC tumors induces their clustering, thereby initiating chronic active signaling activation NF-kB PI3 kinase. Constitutive BCR is essential some GCB but primarily activates We devised genome-wide CRISPR-Cas9 screens to identify regulators IRF4, a direct transcriptional target an indicator...
<p>Supplemental Figure 1. IRF4-GFP knock-in reporter cell lines. Supplemental 2. CRISPR screen in adult T-cell lymphoma and controls. 3. The OST is essential for DLBCL. 4. role of the complex radiation chimeras. 5. B-cell receptor glycosylated by complex. 6. deglycosylation leads to higher surface expression. 7. signaling changes proximal BCR components. 8. recruitment CD22 on alterations GCB 9. internalization My-T-BCR formation glycosylation deficient cells. 10. NGI-1 synergizes with...
<p>Supplemental Figure 1. IRF4-GFP knock-in reporter cell lines. Supplemental 2. CRISPR screen in adult T-cell lymphoma and controls. 3. The OST is essential for DLBCL. 4. role of the complex radiation chimeras. 5. B-cell receptor glycosylated by complex. 6. deglycosylation leads to higher surface expression. 7. signaling changes proximal BCR components. 8. recruitment CD22 on alterations GCB 9. internalization My-T-BCR formation glycosylation deficient cells. 10. NGI-1 synergizes with...
<div>Abstract<p>Diffuse large B-cell lymphoma (DLBCL) can be subdivided into the activated (ABC) and germinal center B cell–like (GCB) subtypes. Self-antigen engagement of receptors (BCR) in ABC tumors induces their clustering, thereby initiating chronic active signaling activation NF-κB PI3 kinase. Constitutive BCR is essential some GCB but primarily activates We devised genome-wide CRISPR–Cas9 screens to identify regulators IRF4, a direct transcriptional target an indicator...
<div>Abstract<p>Diffuse large B-cell lymphoma (DLBCL) can be subdivided into the activated (ABC) and germinal center B cell–like (GCB) subtypes. Self-antigen engagement of receptors (BCR) in ABC tumors induces their clustering, thereby initiating chronic active signaling activation NF-κB PI3 kinase. Constitutive BCR is essential some GCB but primarily activates We devised genome-wide CRISPR–Cas9 screens to identify regulators IRF4, a direct transcriptional target an indicator...
<p>Supplemental Figure 1. IRF4-GFP knock-in reporter cell lines. Supplemental 2. CRISPR screen in adult T-cell lymphoma and controls. 3. The OST is essential for DLBCL. 4. role of the complex radiation chimeras. 5. B-cell receptor glycosylated by complex. 6. deglycosylation leads to higher surface expression. 7. signaling changes proximal BCR components. 8. recruitment CD22 on alterations GCB 9. internalization My-T-BCR formation glycosylation deficient cells. 10. NGI-1 synergizes with...
<p>Supplemental Figure 1. IRF4-GFP knock-in reporter cell lines. Supplemental 2. CRISPR screen in adult T-cell lymphoma and controls. 3. The OST is essential for DLBCL. 4. role of the complex radiation chimeras. 5. B-cell receptor glycosylated by complex. 6. deglycosylation leads to higher surface expression. 7. signaling changes proximal BCR components. 8. recruitment CD22 on alterations GCB 9. internalization My-T-BCR formation glycosylation deficient cells. 10. NGI-1 synergizes with...