Ask about this productRelated genes to: SH3BP4 antibody
- Gene:
- MACC1 NIH gene
- Name:
- MET transcriptional regulator MACC1
- Previous symbol:
- -
- Synonyms:
- 7A5, SH3BP4L
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2008-10-14
- Date modifiied:
- 2018-08-15
- Gene:
- SH3BP4 NIH gene
- Name:
- SH3 domain binding protein 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q37.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-26
- Date modifiied:
- 2016-10-05
Related products to: SH3BP4 antibody
Related articles to: SH3BP4 antibody
- Identification of cancer metastasis-relevant molecular networks is desired to provide the basis for understanding and developing intervention strategies. Here we address the role of GIPC1 in the process of MACC1-driven metastasis. MACC1 is a prognostic indicator for patient metastasis formation and metastasis-free survival. MACC1 controls gene transcription, promotes motility, invasion and proliferation of colon cancer cells , and causes tumor growth and metastasis in mice. - Source: PubMed
Publication date: 2023/12/08
Siegel FranziskaSchmidt HannesJuneja ManishaSmith JaniceHerrmann PiaKobelt DennisSharma KamalFichtner IdunaWalther WolfgangDittmar GunnarVolkmer RudolfRathjen Fritz GSchlag Peter MStein Ulrike - Metastasis Associated in Colon Cancer 1 (MACC1) is a novel prognostic, predictive and causal biomarker for tumor progression and metastasis in many cancer types, including colorectal cancer. Besides its clinical value, little is known about its molecular function. Its similarity to SH3BP4, involved in regulating uptake and recycling of transmembrane receptors, suggests a role of MACC1 in endocytosis. By exploring the MACC1 interactome, we identified the clathrin-mediated endocytosis (CME)-associated proteins CLTC, DNM2 and AP-2 as MACC1 binding partners. We unveiled a MACC1-dependent routing of internalized transferrin receptor towards recycling. Elevated MACC1 expression caused also the activation and internalization of EGFR, a higher rate of receptor recycling, as well as earlier and stronger receptor activation and downstream signaling. These effects are limited by deletion of CME-related protein interaction sites in MACC1. Thus, MACC1 regulates CME and receptor recycling, causing increased growth factor-mediated downstream signaling and cell proliferation. This novel mechanism unveils potential therapeutic intervention points restricting MACC1-driven metastasis. - Source: PubMed
Publication date: 2021/01/20
Imbastari FrancescaDahlmann MathiasSporbert AnjeMattioli Camilla CiolliMari TommasoScholz FlorianTimm LenaTwamley ShaileyMigotti RebekkaWalther WolfgangDittmar GunnarRehm ArminStein Ulrike - We recently identified the metastasis-associated in colon cancer 1 (MACC1) gene by a genome-wide search for differentially expressed genes in human colon cancer tissues, metastases, and normal tissues. Based on MACC1 expression in primary colon cancers, which did not present with metastases, our negative and positive prediction for metachronous metastasis was correct in 80% and 74% of cases, respectively. The 5-year-survival was 80% for MACC1 low expressors, but 15% for individuals who showed high MACC1 expression in their primary tumors. MACC1 induces migration, invasion and proliferation in cell culture, and liver and lung metastases in xenograft models. Here, we describe features of MACC1 beyond its utility as an indicator of metastasis. We elucidate its genomic localization and organization, its predicted splice variants, and single nucleotide polymorphisms. We discuss the MACC1 protein domain structure, posttranslational modifications, its conservation through evolution, and some family ties to SH3BP4. Furthermore, we summarize the predicted expressions of MACC1 in normal and malignant human tissues. We also evaluate the MACC1 levels in the context of one of its transcriptional targets, the receptor tyrosine kinase Met that activates the hepatocyte growth factor/Met signaling pathway, leading to enhanced cell motility, invasion, and metastasis. - Source: PubMed
Publication date: 2009/09/30
Stein UlrikeDahlmann MathiasWalther Wolfgang