Effects of an S-adenosyl-l-homocysteine hydrolase inhibitor on murine macrophage activation and function

Lambert, Laurie E.; Frondorf, Kathleen; Berling, Jennifer S.; Wolos, Jeffrey A.

doi:10.1016/0162-3109(94)00051-g

Cited by 7 publications

(5 citation statements)

References 18 publications

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“…In the case of real refinery feeds, clays pillared with Al, Zr, or Ti have been used as the acid component of the hydrotreating catalyst formulation. − In these cases and since heavy and residual gas oils contain high levels of sulfur, the preferred hydrogenating−dehydrogenating functions (HDF) will be Ni-Co/Mo-W. A catalyst could then be prepared in which the metals are incorporated into the Al 2 O 3 component of the catalyst, and this will be well mixed with the acid PLS component. There is no doubt that if this preparation procedure is selected, it is necessary to ensure that the distance between the HDF and the acid sites should be minimized, otherwise a fast deactivation of the catalyst by coking will occur.…”

Section: Catalytic Activity Of Acid Plsmentioning

confidence: 99%

From Microporous to Mesoporous Molecular Sieve Materials and Their Use in Catalysis

1997

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Section: Catalytic Activity Of Acid Plsmentioning

confidence: 99%

From Microporous to Mesoporous Molecular Sieve Materials and Their Use in Catalysis

1997

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“…Thus, several compounds reduced the production of TNF-a by endotoxin-treated macrophages and protected mice against endotoxin challenge (Parmely et al, 1993;Jeong et al, 1996). Adenosine analogs also inhibited the activation of T cells and decreased the phagocytic activity of macrophages (Sung and Silverstein, 1985;Wolos et al, 1993a,b;Lambert et al, 1995). Some studies have shown a positive correlation between the SAH/SAM ratio and changes in a given cellular function, but none has yet identified the mechanism by which the drugs produce their effect.…”

Section: Discussionmentioning

confidence: 99%

3-Deazaneplanocin A induces massively increased interferon-α production in Ebola virus-infected mice

et al. 2002

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3-Deazaneplanocin A, an analog of adenosine, is a potent inhibitor of Ebola virus replication. A single dose early in infection prevents illness and death in Ebola virus-infected mice. The ability of this and similar compounds to block both RNA and DNA viruses has been attributed to the inhibition of a cellular enzyme, S-adenosylhomocysteine hydrolase (SAH), indirectly resulting in reduced methylation of the 5% cap of viral messenger RNA. However, we found that the protective effect of the drug resulted from massively increased production of interferon-a in Ebola-infected, but not uninfected mice. Peak interferon levels increased with the extent of disease at the time of treatment, indicating that production was boosted only in virus-infected cells. Ebola virus has been shown to suppress innate antiviral mechanisms of the type I interferon response. 3-Deazaneplanocin A appears to reverse such suppression, restricting viral dissemination. Further development should focus on identifying adenosine analogues that produce a similar effect in Ebola virus-infected primates. Published by Elsevier Science B.V.

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“…We recently confirmed those findings and further demonstrated that a reversible SAHase inhibitor (DZ2002) could significantly reduce the severity of experimental autoimmune encephalomyelitis (EAE) [10]. We [8] and others have also suggested a key role for methylation in several other immune cell types, including B cells and macrophages [11; 12]. …”

Section: Introductionmentioning

confidence: 55%

“…We [8; 9; 10] and others [11; 12; 13] have demonstrated a requirement for methylation in T cell signaling pathways. Despite being appropriately phosphorylated, Vav1, a key T cell receptor (TCR) signaling molecule requires arginine methylation for nuclear localization and induction of IL-2 in vitro [14; 15].…”

Section: Introductionmentioning

confidence: 99%

Critical role of transmethylation in TLR signaling and systemic lupus erythematosus

Tardif

Manenkova

Berger

et al. 2013

Clinical Immunology

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Post-translational protein modifications can play a significant role in immune cell signaling. Recently, we showed that inhibition of transmethylation curtails experimental autoimmune encephalomyelitis, notably by reducing T cell receptor (TCR)-induced activation of CD4+ T cells. Here, we demonstrate that transmethylation inhibition by a reversible S-adenosyl-l-homocysteine hydrolase inhibitor (DZ2002) led to immunosuppression by reducing TLR-, B cell receptor (BCR)- and TCR-induced activation of immune cells, most likely by blocking NF-κB activity. Moreover, prophylactic treatment with DZ2002 prevented lupus-like disease from developing in both BXSB and MRL-Faslpr mouse models. DZ2002 treatment initiated during active disease significantly improved outcomes in both in vivo models, suggesting methylation inhibition as a novel approach for the treatment of autoimmune/inflammatory diseases.

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Effects of an S-adenosyl-l-homocysteine hydrolase inhibitor on murine macrophage activation and function

Cited by 7 publications

References 18 publications

From Microporous to Mesoporous Molecular Sieve Materials and Their Use in Catalysis

From Microporous to Mesoporous Molecular Sieve Materials and Their Use in Catalysis

3-Deazaneplanocin A induces massively increased interferon-α production in Ebola virus-infected mice

Critical role of transmethylation in TLR signaling and systemic lupus erythematosus

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