Anti-OLFM4 polyclonal antibody (DPABH-22388)

Rabbit anti-Human OLFM4 (aa 400-450) polyclonal antibody for IHC-P, WB

Specifications


Host Species
Rabbit
Antibody Isotype
IgG
Species Reactivity
Human
Immunogen
Synthetic peptide corresponding to a region within internal sequence amino acids 400-450 (ASTGNMVISK LNDTTLQVLN TWYTKQYKPS ASNAFMVCGV LYATRTMNTR T) of Human OLFM4, conjugated to KLH.
Conjugate
Unconjugated

Applications


Application Notes
IHC-P: 5 μg/ml; WB: 0.5 - 2 μg/ml.
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
OLFM4; olfactomedin 4; olfactomedin-4; GC1; GW112; OlfD
Entrez Gene ID
UniProt ID

Citations


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References


Olfactomedin-related proteins 4 (OLFM4) expression is involved in early gastric carcinogenesis and of prognostic significance in advanced gastric cancer

VIRCHOWS ARCHIV

Authors: Jang, Bo Gun; Lee, Byung Lan; Kim, Woo Ho

Olfactomedin 4 (OLFM4) has been demonstrated to be upregulated in various cancers and involved in many cellular processes such as cell adhesion, apoptosis, and cell proliferation. In gastric cancer, clinicopathological relevance of OLFM4 expression has been reported. However, there are few studies showing how expression of OLFM4 evolves during multistep gastric carcinogenesis. In this study, we investigated OLFM4 expression during gastric carcinogenesis using RNA in situ hybridization (ISH). We found that OLFM4 expression is absent in normal gastric mucosa, begins to appear at the isthmus region in gastric glands in chronic gastritis, and is remarkably increased in intestinal metaplasia (IM). Interestingly, gastric-type glands around IM frequently expressed OLFM4 before CDX2 was expressed, suggesting that OLFM4 might be involved in regulating CDX2 expression. However, overexpression of OLFM4 failed to induce CDX2 transcription. All gastric adenomas were strongly positive for OLFM4. OLFM4 expression was higher in intestinal type, well to moderately differentiated and early-stage adenocarcinomas, and decreased in poorly differentiated and advanced-stage gastric cancer (GC). Although OLFM4 expression had no prognostic value for GC overall (P = 0.441), it was associated with poor survival of GC in stage II, III, and IV (P = 0.018), suggesting that OLFM4 expression has prognostic significance for late-stage GC. Our findings suggest that OLFM4 is not only involved in early stages of gastric carcinogenesis but also a useful prognostic marker for advanced GC, which is encouraging for further studies exploring OLFM4 as a potential target for therapy of GC.

NLRX1 Acts as an Epithelial-Intrinsic Tumor Suppressor through the Modulation of TNF-Mediated Proliferation

CELL REPORTS

Authors: Tattoli, Ivan; Killackey, Samuel A.; Foerster, Elisabeth G.; Molinaro, Raphael; Maisonneuve, Charles; Rahman, Muhammed A.; Winer, Shawn; Winer, Daniel A.; Streutker, Catherine J.; Philpott, Dana J.; Girardin, Stephen E.

The mitochondrial Nod-like receptor protein NLRX1 protects against colorectal tumorigenesis through mechanisms that remain unclear. Using mice with an intestinal epithelial cells (IEC)-specific deletion of Nlrx1, we find that NLRX1 provides an IEC-intrinsic protection against colitis-associated carcinogenesis in the colon. These Nlrx1 mutant mice have increased expression of Tnf, Egf, and Tgfb1, three factors essential for wound healing, as well as increased epithelial proliferation during the epithelial regeneration phase following injury triggered by dextran sodium sulfate. In primary intestinal organoids lacking Nlrx1, stimulation with TNF resulted in exacerbated proliferation and expression of the intestinal stem cell markers Olfm4 and Myb. This hyper-proliferation response was associated with increased activation of Akt and NF-kappa B pathways in response to TNF stimulation. Together, these results identify NLRX1 as a suppressor of colonic tumorigenesis that acts by controlling epithelial proliferation in the intestine during the regeneration phase following mucosal injury.

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