Rabbit Anti-Human B3GALT5 (internal) Polyclonal antibody

Name: Rabbit Anti-Human B3GALT5 (internal) Polyclonal antibody
SKU: DPABH-14855
Rating: 5 (1 reviews)

Rabbit Anti-Human B3GALT5 (internal) Polyclonal antibody for WB

COA

SDS

Datasheet

Key features and details

Specificity: B3GALT5 Antibody detects endogenous levels of total B3GALT5.
Host: Rabbit
Application: WB
Species Reactivity: Human

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Human

Immunogen

A synthesized peptide derived from human B3GALT5, corresponding to a region within the internal amino acids.

Conjugate

Unconjugated

Applications

Application Notes

WB 1:1000-3000

General Notes

This product (Catalog No. DPABH-14855) is a rabbit-derived polyclonal antibody raised against human B3GALT5. It has been affinity purified by Protein A. This gene encodes a member of a family of membrane-bound glycoproteins. The encoded protein may synthesize type 1 Lewis antigens, which are elevated in gastrointestinal and pancreatic cancers. Alternatively spliced transcript variants using multiple alternate promoters have been observed for this gene.
DPABH-14855 is suitable for use in WB 1 (1000-3000) application.
DPABH-14855 is supplied as a liquid formulation in Phosphate buffered saline, pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% 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

Entrez Gene ID

10317

UniProt ID

Q9Y2C3

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Long noncoding RNA B3GALT5-AS1 suppresses colon cancer liver metastasis via repressing microRNA-203

AGING-US

Authors: Wang, Liang; Wei, Zhewei; Wu, Kaiming; Dai, Weigang; Zhang, Changhua; Peng, Jianjun; He, Yulong

Abstract

Long noncoding RNAs (lncRNAs) are implicated in various cancers, including colon cancer. Liver metastasis is the main cause of colon cancer-related death. However, the roles of lncRNAs in colon cancer liver metastasis are still largely unclear. In this study, we identified a novel lncRNA B3GALT5-AS1, which is reduced in colon cancer tissues and further reduced in colon cancer liver metastasis tissues. Reduced expression of B3GALT5-AS1 is associated with liver metastasis and poor outcome of colon cancer patients. Gain-of-function and loss-offunction assays revealed that B3GALT5-AS1 inhibited proliferation but promoted migration and invasion of colon cancer cells. Further investigation revealed that B3GALT5-AS1 directly bound to the promoter of miRNA-203, repressed miR-203 expression, upregulated miR-203 targets ZEB2 and SNAI2, and induced epithelial-to-mesenchymal transition (EMT). In vivo study revealed that B3GALT5-AS1 suppressed colon cancer liver metastasis via its binding on miR-203 promoter and the repression of miR-203. miR-203 is increased and epithelial phenotype is preferred in colon cancer liver metastasis tissues. Collectively, our data revealed the suppressive roles of B3GALT5-AS1/miR-203/EMT regulation axis in colon cancer liver metastasis. Our data suggested that the activating B3GALT5-AS1/miR-203/EMT axis may be potential therapeutic strategy for colon cancer liver metastasis.

SSEA3 and Sialyl Lewis a Glycan Expression Is Controlled by B3GALT5 LTR through Lamin A-NFYA and SIRT1-STAT3 Signaling in Human ES Cells

CELLS

Authors: Cai, Bi-He; Lee, Hsueh-Yi; Chou, Chi-Kan; Wu, Po-Han; Huang, Hsiang-Chi; Chao, Chia-Chun; Chung, Hsiao-Yu; Kannagi, Reiji

Abstract

B3GALT5 is involved in the synthesis of embryonic stem (ES) cell marker glycan, stage-specific embryonic antigen-3 (SSEA3). This gene has three native promoters and an integrated retroviral long terminal repeat (LTR) promoter. We found that B3GALT5-LTR is expressed at high levels in human ES cells. B3GALT5-LTR is also involved in the synthesis of the cancer-associated glycan, sialyl Lewis a. Sialyl Lewis a is expressed in ES cells and its expression decreases upon differentiation. Retinoic acid induced differentiation of ES cells, decreased the short form of NFYA (NFYAs), increased phosphorylation of STAT3, and decreased B3GALT5-LTR expression. NFYAs activated, and constitutively-active STAT3 (STAT3C) repressed B3GALT5-LTR promoter. The NFYAs and STAT3C effects were eliminated when their binding sites were deleted. Retinoic acid decreased the binding of NFYA to B3GALT5-LTR promoter and increased phospho-STAT3 binding. Lamin A repressed NFYAs and SSEA3 expression. SSEA3 repression mediated by a SIRT1 inhibitor was reversed by a STAT3 inhibitor. Repression of SSEA3 and sialyl Lewis a synthesis mediated by retinoic acid was partially reversed by lamin A short interfering RNA (siRNA) and a STAT3 inhibitor. In conclusion, B3GALT5-LTR is regulated by lamin A-NFYA and SIRT1-STAT3 signaling that regulates SSEA3 and sialyl Lewis a synthesis in ES cells, and sialyl Lewis a is also a ES cell marker.