ArticleOncogene2012
Mice deficient in MIM expression are predisposed to lymphomagenesis.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- MTSS1: beyond the integration of actin and membrane dynamics.Cellular and molecular life sciences : CMLS · 2024Review
- Article
- Gene expression changes contribute to stemness and therapy resistance of relapsed acute myeloid leukemia: roles of SOCS2, CALCRL, MTSS1, and KDM6A.Experimental hematology · 2021Review
- MTSS1 inhibits colorectal cancer metastasis by regulating the CXCR4/CXCL12 signaling axis.International journal of molecular medicine · 2021Article
- A Comprehensive Characterization of Monoallelic Expression During Hematopoiesis and LeukemogenesisFrontiers in cell and developmental biology · 2021Article
- Transmembrane adaptor protein WBP1L regulates CXCR4 signalling and murine haematopoiesis.Journal of cellular and molecular medicine · 2020Article
- Missing-in-Metastasis/Metastasis Suppressor 1 Regulates B Cell Receptor Signaling, B Cell Metabolic Potential, and T Cell-Independent Immune Responses.Frontiers in immunology · 2020Article
- Differential interactions of missing in metastasis and insulin receptor tyrosine kinase substrate with RAB proteins in the endocytosis of CXCR4.The Journal of biological chemistry · 2019Article
- Computational analysis of the evolutionarily conserved Missing In Metastasis/Metastasis Suppressor 1 gene predicts novel interactions, regulatory regions and transcriptional control.Scientific reports · 2019Article
- Missing-in-metastasis protein promotes internalization of magnetic nanoparticles via association with clathrin light chain and Rab7.Biochimica et biophysica acta. General subjects · 2019Article
- MTSS1/Src family kinase dysregulation underlies multiple inherited ataxias.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- MicroRNA-324-5p suppresses the migration and invasion of MM cells by inhibiting the SCFOncology letters · 2018Article
- Missing-in-metastasis protein downregulates CXCR4 by promoting ubiquitylation and interaction with small Rab GTPases.Journal of cell science · 2017Article
- Mtss1Leukemia · 2017Article
- Redundant functions of I-BAR family members, IRSp53 and IRTKS, are essential for embryonic development.Scientific reports · 2017Article
- MIM regulates the trafficking of bone marrow cells via modulating surface expression of CXCR4.Leukemia · 2016Article
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- Article
- Identification of the Adapter Molecule MTSS1 as a Potential Oncogene-Specific Tumor Suppressor in Acute Myeloid Leukemia.PloS one · 2015Article
- Dimerization is necessary for MIM-mediated membrane deformation and endocytosis.The Biochemical journal · 2012Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Missing in metastasis (MIM) is a member of newly emerged inverse Bin-Amphiphysin-Rvs (BAR) domain protein family and a putative metastasis suppressor. Although reduced MIM expression has been associated with bladder, breast and gastric cancers, evidence for the role of MIM in tumor progression remains scarce and controversial. Herein we characterized a MIM knockout mouse strain and observed that MIM-deficient mice often developed enlarged spleens. Autopsy and histological analysis revealed that nearly 78% of MIM(-/-) mice developed tumors with features similar to diffuse large B lymphoma during a period from 1 to 2 years. MIM(-/-) mice also exhibited abnormal distribution of B cells in lymphoid organs with decrease in the spleen but increase in the bone marrow and the peripheral blood. Furthermore, the bone marrow of MIM(-/-) mice contained a higher percentage of pre-B2 cells but fewer immature B-cells than wild-type mice. In response to CXCL13, a B-cell chemokine released from splenic stromal cells, MIM-deficient B-cells did not undergo chemotaxis or morphological changes in response to the chemokine and also did not internalize CXCR5, the receptor of CXCL13. Microarray analyses demonstrated that MIM is the only member of the I-BAR domain family that was highly expressed in human B cells. However, low or absent MIM expression was common in either primary B-cell malignancies or established B-cell acute lymphocytic leukemia or lymphomas. Thus, our data demonstrate for the first time an important role for MIM in B-cell development and suggest that predisposition of MIM-null mice to lymphomagenesis may involve aberrant interactions between B lineage cells and the lymphoid microenvironment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.