mProX™ Human TMEM87B Stable Cell Line

Product Information

Target Family

Kinases/Enzyme

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1

Target Classification

Kinase Cell Lines

Gene ID

Human:84910

UniProt ID

Human:Q96K49

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

TMEM87B is a eukaryotic transmembrane protein that has been implicated in various biological processes and diseases. It is part of the TMEM87 protein family, which includes TMEM87A and TMEM87B. TMEM87s have been proposed to have roles in protein transport to and from the Golgi, as mechanosensitive ion channels, and in developmental signaling. Disruption of TMEM87 has been associated with cancers and developmental disorders. Structural and functional analyses suggest that TMEM87A, a member of the TMEM87 protein family, may not function as an ion channel or G-protein coupled receptor. TMEM87A and other structurally related proteins, such as GPR107, GPR108, GPR180, TMEM145, TMEM181, and WLS, share a characteristic domain arrangement and could serve a common role in trafficking membrane-associated cargo. Additionally, TMEM87B has been identified as a potential target of tumor-suppressive miR-30e-3p in head and neck squamous cell carcinoma. It has also been found to be located within the 2q13 critical region associated with congenital heart defects. Further research is needed to fully understand the specific functions and implications of TMEM87B in these contexts.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Taylor Miller (Verified Customer)

Is TMEM87B associated with congenital heart disease? Feb 27 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

Yes, a variant in TMEM87B in patients with a 2q13 microdeletion is associated with congenital heart disease and restrictive cardiomyopathy. Feb 27 2020

chat Skyler Miller (Verified Customer)

How does TMEM87B deficiency impact congenital heart defects? Feb 26 2023

chat Patrick Liam (Creative Biolabs Scientific Support)

Heterozygous loss of TMEM87B is implicated in congenital heart defects and craniofacial abnormalities in 2q13 deletion syndrome. Feb 26 2023

Published Data

Fig.1 Enhanced TMEM87B expression successfully rectified the malfunction observed in V54KO cells.

The enhanced expression of TMEM87A (TM87A) and TMEM87B (TM87B) partially alleviates the delayed protein transport observed in V54KO cells. In transport experiments with VFG-GPI (on the left) or FVG-TM (on the right), V54KO cells exhibited improved protein transport when transiently transfected with the specified genes.

Ref: Hirata, Tetsuya, et al. "Post-Golgi anterograde transport requires GARP-dependent endosome-to-TGN retrograde transport." Molecular biology of the cell 26.17 (2015): 3071-3084.

Pubmed: 26157166

DOI: 10.1091/mbc.E14-11-1568

Research Highlights

M Hoel, Christopher. et al. "Structure of the GOLD-domain seven-transmembrane helix protein family member TMEM87A." eLife, 2022.
Human TMEM87 proteins, TMEM87A and TMEM87B, are intriguing eukaryotic transmembrane proteins implicated in various cellular processes. They have been associated with Golgi protein transport, mechanosensitive ion channel functions, and developmental signaling. Disruption of TMEM87 has links to cancer and developmental disorders. To gain insights into TMEM87A's structure and function, a cryo-EM structure was determined, revealing a unique architecture. Surprisingly, it appears that TMEM87A may not function as an ion channel or G-protein coupled receptor. Additionally, TMEM87A shares structural similarities with seven other human proteins, including WLS, known for its role in membrane trafficking and secretion of lipidated Wnt signaling proteins. This discovery suggests that TMEM87A and its structurally related counterparts could play a shared role in transporting membrane-associated cargo.
M Hoel, Christopher. et al. "Structure of the GOLD-domain seven-transmembrane helix protein family member TMEM87A." eLife, 2022.
Pubmed: 36373655 DOI: 10.7554/eLife.81704

Cai, Zhengyi. et al. "Epigenome-wide DNA methylation study of whole blood in patients with sporadic amyotrophic lateral sclerosis." Chinese medical journal, 2022.
The pathogenesis of sporadic amyotrophic lateral sclerosis (SALS) is influenced by epigenetics, particularly DNA methylation. In light of this, the current study sought to examine the impact of DNA methylation on SALS by analyzing whole blood samples from SALS patients. The findings of this study shed light on the potential role of DNA methylation in the development of SALS, providing valuable insight for future research in this area.
Cai, Zhengyi. et al. "Epigenome-wide DNA methylation study of whole blood in patients with sporadic amyotrophic lateral sclerosis." Chinese medical journal, 2022.
Pubmed: 35853630 DOI: 10.1097/CM9.0000000000002090