GEF-H1 Signaling upon Microtubule Destabilization Is Required for Dendritic Cell Activation and Specific Anti-tumor Responses
Open accessAbstract
Dendritic cell (DC) activation is a critical step for anti-tumor T cell responses. Certain chemotherapeutics can influence DC function. Here we demonstrate that chemotherapy capable of microtubule destabilization has direct effects on DC function; namely, it induces potent DC maturation and elicits anti-tumor immunity. Guanine nucleotide exchange factor-H1 (GEF-H1) is specifically released upon microtubule destabilization and is required for DC activation. In response to chemotherapy, GEF-H1 drives a distinct cell signaling program in DCs dominated by the c-Jun N-terminal kinase (JNK) pathway and AP-1/ATF transcriptional response for control of innate and adaptive immune responses. Microtubule destabilization, and subsequent GEF-H1 signaling, enhances cross-presentation of tumor antigens to CD8 T cells. In absence of GEF-H1, anti-tumor immunity is hampered. In cancer patients, high expression of the GEF-H1 immune gene signature is associated with prolonged survival. Our study identifies an alternate intracellular axis in DCs induced upon microtubule destabilization in which GEF-H1 promotes protective anti-tumor immunity.
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The ability of taxanes to activate RhoA can be relevant for understanding their efficacy in cancer therapy, because RhoA can promote anti-tumour immune responses.
“The ability of taxanes to activate RhoA can be relevant for understanding their efficacy in cancer therapy, because RhoA can promote anti-tumour immune responses 19,75,76 .”
From Taxane-induced conformational changes in the microtubule lattice activate GEF-H1-dependent RhoA signalling (2026) · cites this paper as [19]
The Results (page unavailable) report that the taxanes paclitaxel and docetaxel had no dendritic-cell-stimulatory effects. The Discussion (page unavailable) says the GEF-H1 immune pathway studied is specific to microtubule-destabilizing drugs and is not used by those taxanes. Although it mentions RhoA as a downstream substrate of GEF-H1, it does not establish the proposed taxane–RhoA route to anti-tumour immunity. (LLM, conf=0.86)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredWhen strongly overexpressed, GEF-H1 can induce its preferred lattice conformation, which cannot be altered by paclitaxel.
“This explains why the sensitivity of GEF-H1 to taxanes has been overlooked previously 19 : when strongly overexpressed, GEF-H1 can induce its preferred lattice conformation, which cannot be altered by paclitaxel.”
From Taxane-induced conformational changes in the microtubule lattice activate GEF-H1-dependent RhoA signalling (2026) · cites this paper as [19]
The Results section ('Microtubule Destabilization by MDAs Releases and Activates GEF-H1'; page not provided) reports that taxane did not release GEF-H1 from microtubules in cells overexpressing GEF-H1-GFP. It does not say that strong overexpression induces a preferred lattice conformation or that paclitaxel cannot alter that conformation. (LLM, conf=0.85)
Experimental — accuracy not yet measuredWild-type GEFH1 FL co-localized and bundled microtubules, while the FL-C53R mutant and the FL-αβ, FL-α′β′, and FL-ββ′ mutants showed perturbed microtubule co-localization.
“wild-type FL co-localized and bundled microtubules, consistent with its known microtubule-associated protein behavior”
From Structural basis of microtubule-mediated signal transduction (2026) · cites this paper as [22]
The Results section (“Microtubule Destabilization by MDAs Releases and Activates GEF-H1”; page unavailable) reports GEF-H1 association with microtubules and binding by a purified GEF-H1-derived construct. It does not report that wild-type full-length GEF-H1 bundles microtubules or that the named mutants have perturbed co-localization. The verbatim citing sentence does not mention those mutants. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMicrotubule-destabilizing agents activate GEF-H1 by inducing its unbinding from microtubules.
“As microtubule-destabilizing agents activate GEF-H1 by inducing its unbinding from microtubules 18-21”
From Taxane-induced conformational changes in the microtubule lattice activate GEF-H1-dependent RhoA signalling (2026) · cites this paper as [19]
GEF-H1 is sequestered on microtubules in an inactive form and becomes active upon release from microtubules.
“This effect depends on the RhoA activator guanine nucleotide exchange factor H1 (GEF-H1), which is sequestered on microtubules in an inactive form, but becomes active upon release from microtubules 18-22 .”
From Taxane-induced conformational changes in the microtubule lattice activate GEF-H1-dependent RhoA signalling (2026) · cites this paper as [19]
RhoA activation by microtubule-destabilizing agents depends on GEF-H1.
“This effect depends on the RhoA activator guanine nucleotide exchange factor H1 (GEF-H1), which is sequestered on microtubules in an inactive form, but becomes active upon release from microtubules 18-22 .”
From Taxane-induced conformational changes in the microtubule lattice activate GEF-H1-dependent RhoA signalling (2026) · cites this paper as [19]
Ansamitocin P3-induced dissociation of GEFH1 promotes dendritic cell maturation and antigen cross-presentation.
“ansamitocin P3-induced dissociation of GEFH1 promotes dendritic cell maturation and antigen cross-presentation.22”
From Structural basis of microtubule-mediated signal transduction (2026) · cites this paper as [22]
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- Authors
- Kashyap, A. S., Fernandez-Rodriguez, L., Zhao, Y., Monaco, G., Trefny, M. P., Yoshida, N., Martin, K., Sharma, A., Olieric, N., Shah, P., Stanczak, M., Kirchhammer, N., Park, S.-M., Wieckowski, S., Laubli, H., Zagani, R., Kasenda, B., Steinmetz, M. O., Reinecker, H.-C., & Zippelius, A.
- Affiliations
- Harvard University (US)
- University of Basel (CH)
- Paul Scherrer Institute (CH)
- University Hospital of Basel (CH)
- Corresponding author
- Kashyap, Abhishek S.
- Reinecker, Hans-Christian
- Zippelius, Alfred
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2019-09
- Volume
- 28
- Issue
- 13
- Pages
- 3367-3380.e8
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC6876861
- OpenAlex
- W2975223131
- Cited by
- 76
- References
- 71
- Citations by year
- 2026: 7 · 2025: 17 · 2024: 10 · 2023: 11 · 2022: 12 · 2021: 10 · 2020: 8 · 2019: 1
- FWCI
- 3.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion, cc-by)
- PubMed Central (acceptedVersion, cc-by)
- DORA PSI (Paul Scherrer Institute) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- National Institutes of Health
- Krebsliga Schweiz
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- GEF-H1, microtubule destabilization, dendritic cell activation, dendritic cell maturation, antitumor immunity, chemotherapy, JNK signaling, AP-1 transcription, cross-presentation, CD8+ T cells, tumor antigens, immune-related gene signature, cancer survival
- MeSH terms
- Cell Differentiation, Dendritic Cells, Humans, Microtubules, Neoplasms, Signal Transduction, Rho Guanine Nucleotide Exchange Factors
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