pDP4, a novel glycoprotein secreted by mature granulocytes, is regulated by transcription factor PU.1

Rosenbauer, Frank; Wagner, Katharina; Zhang, Pu; Knobeloch, Klaus–Peter; Iwama, Atsushi; Tenen, Daniel G.

doi:10.1182/blood-2003-08-2688

Cited by 32 publications

(45 citation statements)

References 44 publications

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“…RT-PCR and quantitative RT-PCR to amplify OLFM4 were performed as previously described (8,36). The primers and probes for cytokines and chemokines were all purchased from Applied Biosystems.…”

Section: Methodsmentioning

confidence: 99%

“…However, genetic knock-out mice for myocilin (6) and pancortin-2 (7) demonstrate no obvious phenotypes. OLFM4 is constitutively expressed in neutrophils and the gastrointestinal tract epithelial cells (2,8). A recent study showed that OLFM4 is a target gene of Notch pathway (9), suggesting a potential role for OLFM4 for Notch mediated cell differentiation, proliferation, and immune response to inflammation.…”

Section: Nf-κb | Nucleotide Oligomerization Domain-1 and -2mentioning

confidence: 99%

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Olfactomedin 4 down-regulates innate immunity against Helicobacter pylori infection

Liu

Yan²,

Liu

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

134

152

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Olfactomedin 4 (OLFM4) is a glycoprotein that has been found to be up-regulated in inflammatory bowel diseases and Helicobacter pylori infected patients. However, its role in biological processes such as inflammation or other immune response is not known. In this study, we generated OLFM4 KO mice to investigate potential role(s) of OLFM4 in gastric mucosal responses to H. pylori infection. H. pylori colonization in the gastric mucosa of OLFM4 KO mice was significantly lower compared with WT littermates. The reduced bacterial load was associated with enhanced infiltration of inflammatory cells in gastric mucosa. Production and expression of proinflammatory cytokines/chemokines such as IL-1β, IL-5, IL-12 p70, and MIP-1α was increased in OLFM4 KO mice compared with infected controls. Furthermore, we found that OLFM4 is a target gene of NF-κB pathway and has a negative feedback effect on NF-κB activation induced by H. pylori infection through a direct association with nucleotide oligomerization domain-1 (NOD1) and -2 (NOD2). Together these observations indicate that OLFM4 exerts considerable influence on the host defense against H. pylori infection acting through NOD1 and NOD2 mediated NF-κB activation and subsequent cytokines and chemokines production, which in turn inhibit host immune response and contribute to persistence of H. pylori colonization.NF-κB | nucleotide oligomerization domain-1 and -2

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Section: Methodsmentioning

confidence: 99%

Section: Nf-κb | Nucleotide Oligomerization Domain-1 and -2mentioning

confidence: 99%

Olfactomedin 4 down-regulates innate immunity against Helicobacter pylori infection

Liu

Yan²,

Liu

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

134

152

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“…15 Interestingly, mice are hypomorphic for PU.1, but neither PU.1 þ /À nor PU.1 À/À mice develop AML, suggesting that some remaining activity of Pu.1 is required probably to initiate lineage commitment. 19 The most common translocation in APL fuses the RARA on chromosome 17 to the PML gene on chromosome 15, leading to a PML/RARA fusion protein (accounting for 495% of cases). In the remaining cases of APL, the RARA gene is fused to other genes like PLZF, NPM, NuMA and STAT5, arguing for a common molecular mechanism involving the disruption of the RARA pathway.…”

Section: Tumor Suppressor or Proto-oncogene?mentioning

confidence: 99%

Gatekeeper pathways and cellular background in the pathogenesis and therapy of AML

Cammenga

2005

Leukemia

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Acute myelogenous leukemia (AML) is characterized by the accumulation of immature cells due to disturbed differentiation and proliferation of the myeloid lineage. Genetic alterations affecting transcription factors and receptor tyrosine kinases have been identified in AML and causally linked to the disease. The goal of this review is to address the role of the different genetic alterations in self-renewal and proliferation and to discuss the cellular background in which these events occur during the pathogenesis of AML. Data from AML samples, clinical studies and mouse models for AML will be used to support the different theories regarding the leukemogenesis of AML. Finally, this review wants to highlight the implication of these findings for the therapy of AML.

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“…In the rat eye, the Hnoel-iso gene was more actively expressed in the iris and sclera than in other eye structures (18). The human GW122/ hGC-1 gene, which is also named pDP4 in mice (19) and tiarin in Xenopus (7), is expressed in bone marrow, small intestine, colon, and prostate (20). The myocilin gene is highly expressed in the eye trabecular meshwork and sclera and less actively expressed in several other ocular and non-ocular tissues (1,(21)(22)(23)(24).…”

mentioning

confidence: 99%

“…It has been suggested that the upstream regulatory factor may be essential for the regulation of the MYOCILIN gene (37). The ETSfamily transcription factor PU.1 (Spi-1) may be involved in the regulation of the pDP4 gene in mature mouse granulocytes (19).…”

mentioning

confidence: 99%

The Optimedin Gene Is a Downstream Target of Pax6

Grinchuk

Kozmík²,

Wu³

et al. 2005

Journal of Biological Chemistry

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pDP4, a novel glycoprotein secreted by mature granulocytes, is regulated by transcription factor PU.1

Cited by 32 publications

References 44 publications

Olfactomedin 4 down-regulates innate immunity against Helicobacter pylori infection

Olfactomedin 4 down-regulates innate immunity against Helicobacter pylori infection

Gatekeeper pathways and cellular background in the pathogenesis and therapy of AML

The Optimedin Gene Is a Downstream Target of Pax6

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