Results 1 to 10 of about 3,877 (200)

Tristetraprolin mediates immune evasion of mycobacterial infection in macrophages [PDF]

open access: yesFASEB BioAdvances
Immune evasion of Mycobacterium tuberculosis (Mtb) facilitates intracellular bacterial growth. The mechanisms of immune evasion, however, are still not fully understood.
Jiawei Wei   +10 more
doaj   +5 more sources

Multivalent interactions with CCR4–NOT and PABPC1 determine mRNA repression efficiency by tristetraprolin [PDF]

open access: yesNature Communications
Tristetraprolin family of proteins regulate mRNA stability by binding to specific AU-rich elements in transcripts. This binding promotes the shortening of the mRNA poly(A) tail, or deadenylation, initiating mRNA degradation.
Filip Pekovic   +6 more
doaj   +3 more sources

Exploring the CNOT1(800–999) HEAT Domain and Its Interactions with Tristetraprolin (TTP) as Revealed by Hydrogen/Deuterium Exchange Mass Spectrometry [PDF]

open access: yesBiomolecules
CNOT1, a key scaffold in the CCR4-NOT complex, plays a critical role in mRNA decay, particularly in the regulation of inflammatory responses through its interaction with tristetraprolin.
Maja K. Cieplak-Rotowska   +2 more
doaj   +3 more sources

Lipopolysaccharide regulation of antiinflammatory tristetraprolin family and proinflammatory gene expression in mouse macrophages [PDF]

open access: yesBMC Research Notes
Objective Tristetraprolin (TTP/ZFP36) family proteins exhibit antiinflammatory effects by destabilizing proinflammatory mRNAs. Previous studies showed that bacterial endotoxin lipopolysaccharides (LPS) stimulated TTP and tumor necrosis factor (TNF) gene ...
Heping Cao
doaj   +3 more sources

Myeloid-specific tristetraprolin mitigates postsurgical incisional pain by suppressing proinflammatory responses. [PDF]

open access: yesInflamm Res
Background: Proinflammatory mediators including COX-2, IL-1β, IL-6, and TNF-α, play major roles in the initiation of postsurgical pain. Produced primarily by activated macrophages and microglia, these mediators drive hyperexcitation of nociceptors and ...
Guha A   +9 more
europepmc   +3 more sources

ZIKV induction of tristetraprolin in endothelial and Sertoli cells post-transcriptionally inhibits IFNβ/λ expression and promotes ZIKV persistence

open access: yesmBio, 2023
Zika virus (ZIKV) is a mosquito-borne Flavivirus that persistently infects patients; enters protected brain, placental, and testicular compartments; is sexually transmitted; and causes fetal microcephaly in utero.
William R. Schutt   +4 more
doaj   +2 more sources

Tristetraprolin attenuates schistosomiasis-induced liver fibrosis through m⁶A-mediated regulation of TGF-β1 mRNA stability. [PDF]

open access: yesPLoS Pathog
Inhibiting the activation of hepatic stellate cells (HSCs) represents a key therapeutic strategy for alleviating liver fibrosis induced by schistosomiasis.
Zhao X   +20 more
europepmc   +2 more sources

Tristetraprolin protects against ozone-induced acute lung injury and inflammation in mice. [PDF]

open access: yesJ Immunol
Tristetraprolin (TTP) is an anti‐inflammatory protein that mediates messenger RNA (mRNA) decay of certain transcripts, especially those encoding proinflammatory cytokines.
Lamichhane R   +4 more
europepmc   +2 more sources

Tristetraprolin regulates the skeletal phenotype and osteoclastogenic potential through monocytic myeloid-derived suppressor cells. [PDF]

open access: yesFASEB J, 2023
Tristetraprolin (TTP; also known as NUP475, GOS24, or TIS11), encoded by Zfp36, is an RNA‐binding protein that regulates target gene expression by promoting mRNA decay and preventing translation.
Zhang L   +12 more
europepmc   +2 more sources

Synergistic roles of tristetraprolin family members in myeloid cells in the control of inflammation

open access: yesLife Science Alliance, 2023
Simultaneous deficiency of three tristetraprolin family members in myeloid cells resulted in severe inflammation in mice, suggesting that these three proteins act together to prevent inflammation.
Brittany L Snyder   +7 more
doaj   +2 more sources

Home - About - Disclaimer - Privacy