C57BL/6JCya-Tmem87bem1/Cya
Common Name:
Tmem87b-KO
Product ID:
S-KO-19243
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Tmem87b-KO
Strain ID
KOCMP-72477-Tmem87b-B6J-VB
Gene Name
Product ID
S-KO-19243
Gene Alias
2610301K12Rik; 2810431I02Rik
Background
C57BL/6JCya
NCBI ID
Modification
Conventional knockout
Chromosome
2
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Tmem87bem1/Cya mice (Catalog S-KO-19243) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000110325
NCBI RefSeq
NM_028248
Target Region
Exon 6~8
Size of Effective Region
~1.7 kb
Detailed Document
Overview of Gene Research
TMEM87B is a eukaryotic transmembrane protein. It belongs to the TMEM87 protein family in humans, with TMEM87A being another member [2]. TMEM87s have proposed roles in protein transport to and from the Golgi, and TMEM87B might be involved in endosome-to-TGN retrograde transport as its overexpression in VPS54-KO cells partially restored relevant transport processes [2,3].
In glioma, TMEM87B was identified as a downstream gene of KLF11. KLF11 positively regulates its expression, and high TMEM87B expression in glioma samples indicates a poor prognosis. Elimination of TMEM87B reduces glioma cell proliferation, migration, and tumor spheroid formation, while increasing sensitivity to TMZ. In contrast, overexpression has the opposite effects [1].
In zebrafish, depletion of TMEM87B affects cardiac development, leading to cardiac hypoplasia. This suggests its role in congenital heart disease, especially when combined with 2q13 microdeletion. A patient with such a deletion and a TMEM87B mutation presented with an atrial septal defect and restrictive cardiomyopathy [4,5].
In conclusion, TMEM87B plays important roles in glioma progression and response to treatment, as well as in cardiac development. Studies, including those using zebrafish models with TMEM87B depletion, have revealed its functions in these biological processes and disease-related conditions, providing potential targets for glioma therapy and insights into congenital heart disease mechanisms [1,4,5].
References：
1. Li, Jian, Zong, Hua, Zhao, Xiaoli, Li, Ning, Li, Zhuolun. 2025. KLF11/TMEM87B promoted the occurrence of glioma and decreased TMZ sensitivity. In Cellular signalling, 130, 111651. doi:10.1016/j.cellsig.2025.111651. https://pubmed.ncbi.nlm.nih.gov/39929351/
2. Hoel, Christopher M, Zhang, Lin, Brohawn, Stephen G. 2022. Structure of the GOLD-domain seven-transmembrane helix protein family member TMEM87A. In eLife, 11, . doi:10.7554/eLife.81704. https://pubmed.ncbi.nlm.nih.gov/36373655/
3. Hirata, Tetsuya, Fujita, Morihisa, Nakamura, Shota, Maeda, Yusuke, Kinoshita, Taroh. 2015. Post-Golgi anterograde transport requires GARP-dependent endosome-to-TGN retrograde transport. In Molecular biology of the cell, 26, 3071-84. doi:10.1091/mbc.E14-11-1568. https://pubmed.ncbi.nlm.nih.gov/26157166/
4. Yu, Hung-Chun, Coughlin, Curtis R, Geiger, Elizabeth A, Miyamoto, Shelley D, Shaikh, Tamim H. . Discovery of a potentially deleterious variant in TMEM87B in a patient with a hemizygous 2q13 microdeletion suggests a recessive condition characterized by congenital heart disease and restrictive cardiomyopathy. In Cold Spring Harbor molecular case studies, 2, a000844. doi:10.1101/mcs.a000844. https://pubmed.ncbi.nlm.nih.gov/27148590/
5. Russell, Mark W, Raeker, Maide O, Geisler, Sarah B, Thorsson, Thor, Innis, Jeffrey W. 2014. Functional analysis of candidate genes in 2q13 deletion syndrome implicates FBLN7 and TMEM87B deficiency in congenital heart defects and FBLN7 in craniofacial malformations. In Human molecular genetics, 23, 4272-84. doi:10.1093/hmg/ddu144. https://pubmed.ncbi.nlm.nih.gov/24694933/
Quality Control Standard
Sperm Test
Pre-cryopreservation: Measurement of sperm concentration, determination of sperm viability.
Post-cryopreservation: A vial of cryopreserved sperms is selected for in-vitro fertilization from each batch.
Environmental Standards:SPF
Available Region:Global
Source:Cyagen