PIPages
Labs

Pradipta Ghosh

University of California-San Diego, CA·Biochemistry

Cells constantly sense and respond to signals, and when that signaling goes wrong, disease follows. Cancer cells can keep growing even when outside growth signals run dry.

Fields

Biochemistry

Microbiology & Immunology

Medicine & Clinical Research

Topics

girdin

heterotrimeric G proteins

triple-negative breast cancer

Grants
3 known grants, through Apr 2031

What they work on

  1. Determine how the modular domains of GIV, a scaffold protein linking G-protein switches, drive stem-like states, tumor growth and drug resistance in triple-negative breast cancers, using patient-derived organoids, tissue microarrays and mouse models.
  2. Test how ER+ breast cancer cells gain growth independence by acquiring GIV from neighboring stromal cells, using engineered-circuit cells and quantitative live-cell imaging.
  3. Establish how GIV-expressing cancer cells support GIV-deficient neighbors through paracrine (secreted) signals in mixed tumors, combining experiments with computational modeling.
  4. Identify molecular drivers of macrophage shifts between inflammatory and tolerant states, using semi-high-throughput chemical and genetic screens on mouse and human monocyte-derived macrophages guided by a Boolean Implication Network model.
  5. Test these macrophage polarization drivers in mouse disease models of hyperreactivity and hypertolerance and in human gut organoid co-cultures with microbes and immune cells.
  6. Characterize the direct binding between the bacterial sensor NOD2 and GIV using protein-interaction assays, 3D structural models, FRET imaging, proximity ligation and immunogold electron microscopy.
  7. Define how the NOD2–GIV partnership controls Gαi/cAMP signaling and bacterial clearance, then test it in Salmonella- and Citrobacter-infected mice and in Crohn's patient organoids co-cultured with monocytes.

More about the research

Immune cells called macrophages can become too aggressive or too tolerant, which drives inflammatory disease. A shared thread across these projects is GIV (Gα-interacting vesicle-associated protein), a scaffold protein that links several signaling switches inside the cell. The lab asks how GIV and related signaling networks control cancer growth and macrophage behavior. The work combines cell biology, mouse models, human organoids (miniature lab-grown tissues) and computational analysis of gene expression.

Why it matters

The breast cancer work could reveal new ways to target the stem-like cells that drive tumor growth and drug resistance, in triple-negative and ER+ breast cancer. The macrophage studies could point to therapeutic targets for resetting immune responses in colitis, sepsis and other inflammatory diseases. They could also reveal signaling interfaces lost in Crohn's disease that might be manipulated to treat chronic gut inflammation.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Integrated G Protein Circuitry for Cancer Cell Signaling Autonomy

NIH · May 2026 – Apr 2031

Modulation of Macrophage Polarization by Heterotrimeric G proteins: Implications of Gastrointestinal Inflammation

NIH · May 2019 – Jan 2031

Macrophage Polarization in Response to Infections and Inflammation

NIH · Sep 2020 – Aug 2027

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Ling-shiang Chuang

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Profile perianal fistula tissue from Crohn's disease patients with single-cell multiome ATAC plus transcriptome and spatial transcriptomics, which measure open DNA, gene activity and location cell by cell.

Louis Cohen

Icahn School of Medicine at Mount Sinai, NY·Microbiology & Immunology

Profile the hematopoietic (blood-forming) stem cell and progenitor populations that are associated with treatment-resistant Crohn's disease, drawing on patients who received autologous stem cell transplantation.

The school

University of California-San Diego: 84 labs on PI Pages, $1.9B a year on research, 637 research doctorates a year.

More about University of California-San Diego

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