Jin Huk Choi
University of Texas Southwestern Medical Center, TX·Microbiology & Immunology
Every cell needs ribosomes, the molecular machines that read genetic instructions and build proteins. Immune cells depend on them heavily, because they must divide quickly, mature into specialized types and mount responses against infections.
- Fields
Microbiology & Immunology
Genetics
Biochemistry
- Topics
ribosome biogenesis
Polr1h
RNA polymerase I
- Grants
- 1 known grant, through Apr 2031
What they work on
- Define how the ZFP574–THAP12 complex, a pair of zinc finger proteins found in a mouse mutagenesis screen, supports immune cell development and function by switching on Polr1h, a subunit of the ribosomal RNA-making enzyme RNA Polymerase I.
- Test whether ZFP574–THAP12 control of Polr1h is required for RNA Polymerase I activity, ribosomal RNA synthesis and progression through the G1–S stage of the cell cycle in lymphocytes.
- Evaluate the therapeutic potential of targeting the ZFP574–THAP12–Polr1h pathway in mouse models of leukemia and autoimmune disease.
More about the research
When ribosome production runs too high, it can feed cancer and autoimmunity. When it runs too low, it can cause immune deficiency and a shortage of blood cells, called cytopenia. Still, how immune cells control ribosome production is poorly understood.
Why it matters
Leukemia cells and the overactive lymphocytes in autoimmune disease take over the growth and survival programs that normal immune cells use, and treatments that selectively disrupt these programs are needed. The ZFP574–THAP12 complex, which sustains lymphocyte survival and ribosome production, could become a new drug target for people with leukemia or autoimmune disorders.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Randall Davis
University of Alabama at Birmingham, AL·Microbiology & Immunology
Determine how FCRL1, a B cell surface receptor overproduced in leukemia, influences B cell responses in human and mouse disease models of chronic lymphocytic leukemia and immune tolerance.
Guillermina Lozano
University of Texas MD Anderson Cancer Center, TX·Genetics
Determine the roles of Eda2r, a cell-surface receptor that can trigger apoptosis, in p53-dependent cell outcomes and tumor suppression in mouse models.
Ramiro Verdun
University of Miami, FL·Biochemistry
Determine how bypass of transcription-blocking DNA lesions by RNA Polymerase II, the enzyme that copies genes into RNA, disrupts the cellular response to ultraviolet radiation damage and disturbs normal cell function.
The school
University of Texas Southwestern Medical Center: 40 labs on PI Pages, $869M a year on research, 86 research doctorates a year.
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