The nuclear protein HMGB1 is secreted by monocytes via a non‐classical, vesicle‐mediated secretory pathway
By Stefania Gardella, Cristina Andrei, Denise Ferrera, L. Lotti, M. Torrisi, M. Bianchi, A. Rubartelli. EMBO Reports, 2002
988 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Genetics, Immunology
View Paper: https://www.semanticscholar.org/paper/4033d2fc60bf3faf8b3a50c6d778b0d0a882bcea
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Clinical Biochemistry
In Genetics
In Immunology
Citations in the corpus
- Inflammation and necrosis promote tumour growth (2004, background): “Surprisingly, in these immune-incompetent animals, blocking the expression of this receptor by macrophages enhances TNF productio”
- High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal (2005, background): “HMGB1 is a 'leaderless' cytokine, meaning that it is not translocated directly from the Golgi apparatus to the cell membrane after synthesis as are the haematopoietic cytokines (for example, IL-2, IL-4 and IL-7) but requires specialized means to gain access to the IMMUNOLOGICAL SYNAPSE or to be se”
- High‐mobility group box 1 (HMGB1) protein at the crossroads between innate and adaptive immunity (2007, background): “In the case of myeloid cells, HMGB1 then is concentrated within a subpopulation of ‘secretory’ lysosomes, whose contents are discharged into the extracellular medium when cells receive specific signals (30).”
- Toll-like receptor 4–dependent contribution of the immune system to anticancer chemotherapy and radiotherapy (2007, background): “HMGB1 is a nonhistone chromatin-binding nuclear constituent that is passively released by dying cells and actively secreted by inflammatory APC”
- Feature-based prediction of non-classical and leaderless protein secretion. (2004, background): “Even though this is a nuclear protein, proteins carrying similar domains have been shown to enter the non-classical secretory pathway (Gardella et al., 2002; Nickel, 2003).”
- DAMPening Inflammation by Modulating TLR Signalling (2010, background): “This nonclassical secretion pathway is distinct from the passage through the ER and Golgi taken by signal tagged proteins, instead requiring the microtubule cytoskeleton [180].”
- Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release (2012, background): “HMGB1 is released passively into the extracellular medium during necrosis and is secreted actively by monocytes and macrophages after stimulation with LPS and ATP (Gardella et al., 2002).”
- The inflammatory response to cell death. (2008, background): “In addition to being passively released from necrotic cells, HMGB1 has also recently been found to be released by a non-classical secretion mechanism from a subset of activated leukocytes (monocytes, macrophages, DC and NK cells) (34) (35).”
- HMGB1 Is a Therapeutic Target for Sterile Inflammation and Infection (2011, background): “Active secretion of HMGB1, initiated by cellular signal transduction through plasma membrane receptor interaction with extracellular products, occurs more slowly (2, 8).”
- HMGB1 is an endogenous immune adjuvant released by necrotic cells (2004, background): “In myeloid cells, HMGB1 is secreted through specific organelles, the secretory lysosomes (Gardella et al, 2002), and is extensively acetylated in order to reach them from the nucleus (Bonaldi et al, 2003).”