| 2013 |
CMTM7 promotes EGFR internalization in carcinoma cells, thereby suppressing downstream AKT signaling. Ectopic CMTM7 expression causes G1/S cell cycle arrest associated with upregulation of p27 and downregulation of CDK2 and CDK6. |
Ectopic expression in carcinoma cell lines, cell cycle analysis, Western blot for AKT/p27/CDK2/CDK6, EGFR internalization assay, nude mouse tumor formation |
Oncogene |
Medium |
23893243
|
| 2015 |
CMTM7 knockdown increases EGFR-AKT signaling by reducing EGFR internalization and degradation. Mechanistically, CMTM7 is required for activation of Rab5, a GTPase needed for early endosome fusion; loss of CMTM7 reduces GTP-Rab5 levels. |
Stable shRNA knockdown in NSCLC cells, EGFR internalization/degradation assays, Rab5 activation assay, Western blot for AKT phosphorylation |
Oncotarget |
Medium |
26528697
|
| 2012 |
CMTM7, a tetra-spanning membrane protein, physically associates with surface IgM (BCR) and with BLNK in a membrane fraction; this interaction is augmented after BCR ligation. CMTM7 recruits BLNK to the vicinity of Syk, enabling BLNK phosphorylation and downstream JNK/ERK activation. The C-terminal domain is required for membrane localization and for these functions, while N-terminal deletion mutants retain activity. |
RNAi knockdown in B cells, co-immunoprecipitation (CMTM7-BLNK and CMTM7-sIgM), rescue experiments with deletion mutants, tyrosine phosphorylation assays, JNK/ERK activation assays |
PloS one |
High |
22363743
|
| 2013 |
CMTM7 is required for normal BCR expression and survival specifically in B-1a cells but not B-2 cells. Cmtm7(flox/+) heterozygous reduction leads to decreased BCR surface levels, increased spontaneous apoptosis, impaired IgM secretion, and poor LPS-induced proliferation in B-1a cells. |
Rag1−/− reconstitution with Cmtm7(flox/+) fetal liver cells, flow cytometry for BCR surface expression and cell death, serum IgM measurement, proliferation assays |
International immunology |
Medium |
24080084
|
| 2019 |
Cmtm7 knockout blocks B-1a cell development specifically at the transitional B-1a (TrB-1a) stage, causing slow proliferation and high cell death at that stage. This is a B-cell-intrinsic defect confirmed by bone marrow and fetal liver adoptive transfer and conditional knockout models. Cmtm7-deficient mice produce less IgM and IL-10 and are more susceptible to microbial sepsis. |
Cmtm7 global knockout mice, conditional knockout, bone marrow/fetal liver adoptive transfer, flow cytometry at developmental stages, IgM/IL-10 ELISA, sepsis model |
International immunology |
High |
31081901
|
| 2020 |
CMTM7 is required for TLR agonist-induced plasma cell differentiation in B-1 cells. Loss of Cmtm7 suppresses downregulation of Pax5 and upregulation of Xbp1, Irf4, and Prdm1 (transcription factors governing plasma cell fate), and inhibits p38 phosphorylation. A p38 inhibitor phenocopies Cmtm7 deficiency, placing CMTM7 upstream of p38 in B-1 cell terminal differentiation. |
Cmtm7 knockout mice, in vitro TLR stimulation, flow cytometry for plasma cell markers, Western blot for p38 phosphorylation, p38 inhibitor epistasis experiment, IgM/IL-10 ELISA |
European journal of immunology |
High |
32022930
|
| 2020 |
In splenic B-1a cells, Cmtm7 knockout elevates surface CD5, CD80, and CD86 and enhances tonic BCR signaling at steady state. Cmtm7 deficiency promotes splenic B-1a apoptosis in situ, associated with downregulation of IL-5Rα. Cmtm7 also shapes the IgM heavy-chain repertoire differently in peritoneal vs. splenic B-1a cells. |
Cmtm7 knockout mice, flow cytometry, BCR signaling assays, Igμ repertoire sequencing, apoptosis assays in situ |
Cellular immunology |
Medium |
32305130
|
| 2021 |
Dual knockdown of CMTM6 and CMTM7 significantly reduces PD-L1 surface expression in mesenchymal breast cancer cells, indicating that CMTM7 contributes to maintaining cell-surface PD-L1 during EMT. |
siRNA dual knockdown of CMTM6 and CMTM7 in MCF-7Mes cells, flow cytometry for surface PD-L1 |
Cancers |
Low |
33803139
|
| 2023 |
CMTM7 interacts with CTNNA1 (Catenin Alpha 1) and regulates Wnt/β-catenin signaling in breast cancer cells. A feedback loop comprising miR-182-5p, CMTM7, CTNNA1, β-catenin (CTNNB1), and TCF3 was identified; TCF3 transcriptionally activates miR-182-5p, which targets and represses CMTM7, while CMTM7 suppresses β-catenin/TCF3 output. |
Co-IP (CMTM7-CTNNA1 interaction), luciferase reporter assay (miR-182-5p targeting CMTM7; TCF3 promoter activity on miR-182-5p), ChIP analysis, Western blot, in vitro and in vivo functional assays |
Breast cancer research : BCR |
Medium |
36829181
|
| 2025 |
CMTM7 inhibits TLR4 signaling in macrophages by promoting the interaction between Rab5 and its GEF Gapex5, generating GTP-Rab5, which facilitates TLR4 internalization and degradation, thereby suppressing downstream inflammatory signaling. Myeloid-conditional Cmtm7 knockout mice show exacerbated acute liver injury, and adoptive transfer of CMTM7-overexpressing macrophages is protective. |
Myeloid conditional Cmtm7 knockout mice, Rab5 activation assay (GTP-Rab5), co-immunoprecipitation (Rab5-Gapex5 interaction), TLR4 internalization/degradation assays, LPS/HMGB1 stimulation, adoptive transfer of CMTM7-overexpressing macrophages, ALI mouse model |
Cellular and molecular life sciences : CMLS |
High |
40490565
|
| 2018 |
SOX10 transcriptionally regulates CMTM7 expression in gastric cancer. Overexpression of SOX10 in CMTM7-silenced gastric cancer cells inhibits proliferation and tumor growth, placing CMTM7 downstream of SOX10 in this pathway. |
Bioinformatics, luciferase reporter assay (SOX10 binding to CMTM7 promoter), stable CMTM7 silencing, SOX10 overexpression in CMTM7-knockdown cells, proliferation and in vivo tumor assays |
Biochemical and biophysical research communications |
Medium |
30392914
|
| 2025 |
SOX10 transcriptionally represses CMTM7 in pancreatic cancer (dual-luciferase assay). CMTM7 overexpression inhibits the Wnt/β-catenin pathway and induces ferroptosis in PC cells; silencing CMTM7 reverses the anti-tumor effects of SOX10 knockdown, placing CMTM7 downstream of SOX10 in a Wnt/β-catenin-ferroptosis axis. |
Dual-luciferase reporter assay, shRNA knockdown, CMTM7 overexpression, flow cytometry for apoptosis/ferroptosis markers, Wnt/β-catenin pathway Western blot, tumor-bearing mouse model |
European journal of medical research |
Medium |
39754171
|