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21 in total

1. Hydrogen sulfide is an endogenous potentiator of T cell activation.

Authors: Thomas W Miller; Evelyn A Wang; Serge Gould; Erica V Stein; Sukhbir Kaur; Langston Lim; Shoba Amarnath; Daniel H Fowler; David D Roberts
Journal: J Biol Chem Date: 2011-12-13 Impact factor: 5.157

2. Identification of target actin content and polymerization status as a mechanism of tumor resistance after cytolytic T lymphocyte pressure.

Authors: Soraya Abouzahr; Georges Bismuth; Catherine Gaudin; Oliver Caroll; Peter Van Endert; Abdelali Jalil; Jean Dausset; Isabelle Vergnon; Catherine Richon; Audrey Kauffmann; Jérôme Galon; Graca Raposo; Fathia Mami-Chouaib; Salem Chouaib
Journal: Proc Natl Acad Sci U S A Date: 2006-01-23 Impact factor: 11.205

3. Gelsolin overexpression alters actin dynamics and tyrosine phosphorylation of lipid raft-associated proteins in Jurkat T cells.

Authors: S Celeste Morley; Janice Sung; Guang-Ping Sun; Maria Paola Martelli; Stephen C Bunnell; Barbara E Bierer
Journal: Mol Immunol Date: 2006-12-18 Impact factor: 4.407

Interplay between TCR signalling and actin cytoskeleton dynamics.

1. Hydrogen sulfide is an endogenous potentiator of T cell activation.

2. Identification of target actin content and polymerization status as a mechanism of tumor resistance after cytolytic T lymphocyte pressure.

3. Gelsolin overexpression alters actin dynamics and tyrosine phosphorylation of lipid raft-associated proteins in Jurkat T cells.

Review 4. Immunopathologies linked to integrin signalling.

5. CD47-dependent regulation of H₂S biosynthesis and signaling in T cells.

6. T cell receptor-dependent tyrosine phosphorylation of beta2-chimaerin modulates its Rac-GAP function in T cells.

7. Seven kinds of intermediate filament networks in the cytoplasm of polarized cells: structure and function.

8. Acute endotoxin-induced thymic atrophy is characterized by intrathymic inflammatory and wound healing responses.

Review 9. Age-related defects in the cytoskeleton signaling pathways of CD4 T cells.

10. Cholera toxin B accelerates disease progression in lupus-prone mice by promoting lipid raft aggregation.