Rabbit Anti-Human OLFM4 (C-terminal) Polyclonal antibody

Name: Rabbit Anti-Human OLFM4 (C-terminal) Polyclonal antibody
SKU: DPABH-03567
Rating: 5 (1 reviews)

Rabbit Anti-Human OLFM4 (C-terminal) Polyclonal antibody for WB

COA

SDS

Datasheet

Key features and details

Target: OLFM4
Host: Rabbit
Application: WB
Species Reactivity: Human

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Human

Immunogen

Fusion protein corresponding to residues near the C terminal of human olfactomedin 4

Conjugate

Unconjugated

Applications

Application Notes

WB: 1:200-1:1000

General Notes

This product (Catalog No. DPABH-03567) is a rabbit-derived polyclonal antibody raised against human OLFM4. It has been affinity purified by Protein A. This gene was originally cloned from human myeloblasts and found to be selectively expressed in inflammed colonic epithelium. This gene encodes a member of the olfactomedin family. The encoded protein is an antiapoptotic factor that promotes tumor growth and is an extracellular matrix glycoprotein that facilitates cell adhesion.
DPABH-03567 is suitable for use in Western blot (WB) (1:200–1:1,000) application.
DPABH-03567 is supplied as a liquid formulation in pH7.4 PBS, 0.05% sodium azide, 40% Glycerol. For long-term storage, keep at −20 °C. For short-term use, store at 2–8 °C. Avoid repeated freeze–thaw cycles to maintain antibody integrity and performance.

Target

Alternative Names

GC1; OLM4; OlfD; GW112; hGC-1; hOLfD; UNQ362; bA209J19.1

Entrez Gene ID

10562

UniProt ID

Q6UX06

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

EVI2B, ATP2A2, S100B, TM4SF3, and OLFM4 As Potential Prognostic Markers for Postoperative Taiwanese Colorectal Cancer Patients

DNA AND CELL BIOLOGY

Authors: Huang, Ming-Yii; Wang, Hwei-Ming; Tok, Teck-Siang; Chang, Hui-Jen; Chang, Ming-Sung; Cheng, Tian-Lu; Wang, Jaw-Yuan; Lin, Shiu-Ru

Abstract

Undetected micrometastasis may play a key role in the early relapse of colorectal cancer (CRC) patients. The aim of this study was to detect circulating tumor cells (CTCs) for predicting early relapse of CRC patients by a weighted enzymatic chip array (WEnCA) and analyze 15 candidate genes associated with CRC carcinogenesis. The genes of 105 postoperative CRC patients were analyzed by membrane array and direct sequencing. We constructed a WEnCA platform including five prognosis-related genes and analyzed the detection rate of WEnCA for CTCs in 30 clinically confirmed CRC relapse patients. Postoperative relapse was significantly correlated with gene overexpression, including EVI2B (p = 0.001, OR = 4.622), ATP2A2 (p = 0.006, OR = 4.688), S100B (p = 0.001, OR = 11.521), TM4SF3 (p = 0.001, OR = 6.756), and OLFM4 (p = 0.008, OR = 3.545). Using WEnCA (weighting score of each gene: 5 to EVI2B, 5 to ATP2A2, 12 to S100B, 7 to TM4SF3, and 4 to OLFM4), we could detect CTCs presenting these genotypes in relapsed CRC patients. The sensitivity, specificity, and accuracy were 94.7%, 93.5%, and 97%, respectively. The results of the present study suggest that EVI2B, ATP2A2, S100B, TM4SF3, and OLFM4 could be potential prognostic markers for CRC patients.

Mitochondrial function controls intestinal epithelial stemness and proliferation

NATURE COMMUNICATIONS

Authors: Berger, Emanuel; Rath, Eva; Yuan, Detian; Waldschmitt, Nadine; Khaloian, Sevana; Allgaeuer, Michael; Staszewski, Ori; Lobner, Elena M.; Schoettl, Theresa; Giesbertz, Pieter; Coleman, Olivia I.; Prinz, Marco; Weber, Achim; Gerhard, Markus; Klingenspor, Martin; Janssen, Klaus-Peter; Heikenwalder, Mathias; Haller, Dirk

Abstract

Control of intestinal epithelial stemness is crucial for tissue homeostasis. Disturbances in epithelial function are implicated in inflammatory and neoplastic diseases of the gastrointestinal tract. Here we report that mitochondrial function plays a critical role in maintaining intestinal stemness and homeostasis. Using intestinal epithelial cell (IEC)-specific mouse models, we show that loss of HSP60, a mitochondrial chaperone, activates the mitochondrial unfolded protein response (MT-UPR) and results in mitochondrial dysfunction. HSP60-deficient crypts display loss of stemness and cell proliferation, accompanied by epithelial release of WNT10A and RSPO1. Sporadic failure of Cre-mediated Hsp60 deletion gives rise to hyperproliferative crypt foci originating from OLFM4(+) stem cells. These effects are independent of the MT-UPR-associated transcription factor CHOP. In conclusion, compensatory hyperproliferation of HSP60(+) escaper stem cells suggests paracrine release of WNT-related factors from HSP60-deficient, functionally impaired IEC to be pivotal in the control of the proliferative capacity of the stem cell niche.