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C57BL/6JCya-Gpr65em1flox/Cya
Common Name:
Gpr65-flox
Product ID:
S-CKO-02714
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
Price:
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Basic Information
Strain Name
Gpr65-flox
Strain ID
CKOCMP-14744-Gpr65-B6J-VA
Gene Name
Gpr65
Product ID
S-CKO-02714
Gene Alias
Dig1; Gpcr25; TDAG8
Background
C57BL/6JCya
NCBI ID
14744
Modification
Conditional knockout
Chromosome
12
Phenotype
MGI:108031
Document
Click here to download >>
Application
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Rare Disease Data Center >>
Note
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Gpr65em1flox/Cya mice (Catalog S-CKO-02714) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000075072
NCBI RefSeq
NM_008152
Target Region
Exon 2
Size of Effective Region
~3.6 kb
Detailed Document
Click here to download >>
Overview of Gene Research
Gpr65, a G-protein coupled receptor, is a proton-sensing receptor. It is involved in regulating multiple pathophysiological processes through various signaling pathways such as Gαq-Ca2+-JNK/NF-κB, cAMP-PKA-C-Raf-ERK1/2-LKB1, and cAMP/PKA/CREB [1,2,5]. It plays a significant role in maintaining tissue homeostasis and is associated with multiple diseases [1-5,7-10]. Genetic models, especially knockout (KO) and conditional knockout (CKO) mouse models, have been crucial in understanding its functions.

In liver fibrosis, Gpr65-deficient mice showed alleviated liver inflammation, injury, and fibrosis induced by bile duct ligation or carbon tetrachloride treatment. Gpr65 in hepatic macrophages was upregulated in fibrotic livers, and its knockout's protective effect was mainly mediated by bone marrow-derived macrophages. Mechanistically, Gpr65 regulated the activation of hepatic stellate cells and damage of hepatocytes via the Gαq-Ca2+-JNK/NF-κB and Gαq-Ca2+-MLK3-MKK7-JNK pathways [1].

In intestinal mucosal inflammation, conditional knockout of Gpr65 in CD4+ T cells ameliorated trinitrobenzene sulfonic acid-induced acute murine colitis and chronic colitis in Rag1-/-mice. Gpr65 promoted Th1 and Th17 cell differentiation by downregulating NUAK2 [2].

In obesity-associated cancers like colorectal and hepatocellular carcinoma, macrophage-specific Gpr65 promoted tumor growth [3].

In the gut, Gpr65 deletion in intestinal epithelial cells abrogated antimicrobial programs, making mice prone to colitis [4].

In glioma, Gpr65 on tumor-associated macrophages promoted tumor progression by sensing lactate and releasing HMGB1 [5].

In trophoblast cells, overexpression of Gpr65 inhibited adhesion, migration, and invasion under acidic conditions [6].

In glioma, Gpr65 was identified as a hub gene in M2 macrophage-related modules, and its inhibition reduced macrophage polarization [7].

Delayed treatment with the Gpr65 agonist BTB09089 promoted neurorehabilitation after ischemic stroke in wild-type but not Gpr65-/-mice [8].

In B-cell acute lymphoblastic leukemia, Gpr65 inactivation in tumor cells led to CAR T-cell resistance [9].

In conclusion, Gpr65 is a key regulator in multiple biological processes. Studies using KO and CKO mouse models have revealed its role in liver fibrosis, intestinal inflammation, obesity-associated cancers, gut mucosal homeostasis, glioma progression, trophoblast cell function, neurorehabilitation after stroke, and CAR T-cell therapy response in leukemia. These findings provide potential therapeutic targets for related diseases.

References:
1. Zhang, Kun, Zhang, Meng-Xia, Meng, Xiao-Xiang, Han, Tao, Hong, Wei. 2023. Targeting GPR65 alleviates hepatic inflammation and fibrosis by suppressing the JNK and NF-κB pathways. In Military Medical Research, 10, 56. doi:10.1186/s40779-023-00494-4. https://pubmed.ncbi.nlm.nih.gov/38001521/
2. Lin, Ritian, Wu, Wei, Chen, Huimin, Sun, Mingming, Liu, Zhanju. . GPR65 promotes intestinal mucosal Th1 and Th17 cell differentiation and gut inflammation through downregulating NUAK2. In Clinical and translational medicine, 12, e771. doi:10.1002/ctm2.771. https://pubmed.ncbi.nlm.nih.gov/35343079/
3. Bagchi, Sreya, Yuan, Robert, Huang, Han-Li, Plevritis, Sylvia, Engleman, Edgar G. 2024. The acid-sensing receptor GPR65 on tumor macrophages drives tumor growth in obesity. In Science immunology, 9, eadg6453. doi:10.1126/sciimmunol.adg6453. https://pubmed.ncbi.nlm.nih.gov/39423285/
4. Li, Gengfeng, Lin, Jian, Gao, Xiang, Fang, Leilei, Liu, Zhanju. 2023. Intestinal epithelial pH-sensing receptor GPR65 maintains mucosal homeostasis via regulating antimicrobial defense and restrains gut inflammation in inflammatory bowel disease. In Gut microbes, 15, 2257269. doi:10.1080/19490976.2023.2257269. https://pubmed.ncbi.nlm.nih.gov/37749885/
5. Yan, Chaolong, Yang, Zijiang, Chen, Pin, Huang, Wei, Zhang, Xiaobiao. 2024. GPR65 sensing tumor-derived lactate induces HMGB1 release from TAM via the cAMP/PKA/CREB pathway to promote glioma progression. In Journal of experimental & clinical cancer research : CR, 43, 105. doi:10.1186/s13046-024-03025-8. https://pubmed.ncbi.nlm.nih.gov/38576043/
6. Mao, Jia, Feng, Ying, Zheng, Yayun, Zhu, Xiaofeng, Ma, Fang. 2023. GPR65 inhibits human trophoblast cell adhesion through upregulation of MYLK and downregulation of fibronectin via cAMP-ERK signaling in a low pH environment. In Cell communication and signaling : CCS, 21, 238. doi:10.1186/s12964-023-01249-3. https://pubmed.ncbi.nlm.nih.gov/37723567/
7. Fan, Jikang, Liu, Jie, Zhang, Bin, Li, Tao, Yang, Xuejun. 2024. GPR65 contributes to constructing immunosuppressive microenvironment in glioma. In Neurosurgical review, 47, 417. doi:10.1007/s10143-024-02633-4. https://pubmed.ncbi.nlm.nih.gov/39123083/
8. Chen, Ru, Zhang, Meng-Qi, Miao, Yu-Lu, Zhang, Yu, Fan, Yan-Ying. 2024. Targeting Neuronal GPR65 With Delayed BTB09089 Treatment Improves Neurorehabilitation Following Ischemic Stroke. In Stroke, 55, 2151-2162. doi:10.1161/STROKEAHA.124.046954. https://pubmed.ncbi.nlm.nih.gov/38946544/
9. Mavuluri, Jayadev, Dhungana, Yogesh, Jones, Lindsay L, Yu, Jiyang, Geiger, Terrence L. . GPR65 Inactivation in Tumor Cells Drives Antigen-Independent CAR T-cell Resistance via Macrophage Remodeling. In Cancer discovery, 15, 1018-1036. doi:10.1158/2159-8290.CD-24-0841. https://pubmed.ncbi.nlm.nih.gov/39998425/
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
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