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Actin filament associated protein 1

AFAP, AFAP-110, actin filament-associated protein AFAP-110
The protein encoded by this gene is a Src binding partner. It may represent a potential modulator of actin filament integrity in response to cellular signals, and may function as an adaptor protein by linking Src family members and/or other signaling proteins to actin filaments. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Aug 2008] (from NCBI)
Top mentioned proteins: APC, Actin, Src, AGE, CAN
Papers on AFAP
Mitochondrial variants in MT-CO2 and D-loop instability are involved in MUTYH-associated polyposis.
Venesio et al., Torino, Italy. In J Mol Med (berl), Nov 2015
We compared the breadth of somatic variants across the mitochondrial genome of MUTYH-associated polyposis (MAP) patients with homogeneous groups of classical/attenuated familial adenomatous polyposis (FAP/AFAP) and sporadic cases.
Regulation of sarcoma cell migration, invasion and invadopodia formation by AFAP1L1 through a phosphotyrosine-dependent pathway.
Ingley et al., Australia. In Oncogene, Aug 2015
We have identified a novel pathway that directs Lyn/Src family tyrosine kinase signals to the invadopodia to regulate sarcoma cell invasion via the molecule AFAP-1-like-1 (AFAP1L1), a new member of the AFAP (actin filament-associated protein) family.
Novel Missense Mutation at Codon 2774 (C.8321 G>A) p.S2774N of APC Gene in a Denovo Case of Familial Adenomatous Polyposis.
Zali et al., Tehrān, Iran. In Arch Iran Med, Jul 2015
A milder form of FAP with fewer numbers of polyps (< 100) is Attenuated FAP (AFAP) and in comparison with classical FAP, it usually diagnosed at an older age.
Attenuated familial adenomatous polyposis manifests as autosomal dominant late-onset colorectal cancer.
Berg et al., Cambridge, United Kingdom. In Eur J Hum Genet, 2014
In this study, we estimated CRC risks for carriers of a novel germline mutation in the APC gene that causes attenuated FAP (AFAP).
Promoter-specific alterations of APC are a rare cause for mutation-negative familial adenomatous polyposis.
Peltomäki et al., Helsinki, Finland. In Genes Chromosomes Cancer, 2014
n familial adenomatous polyposis (FAP), 20% of classical and 70% of attenuated/atypical (AFAP) cases remain mutation-negative after routine testing; yet, allelic expression imbalance may suggest an APC alteration.
Molecular analysis of the APC gene in Sicilian patients with familial adenomatous polyposis (F.A.P.).
Travali et al., Catania, Italy. In Int J Surg, 2013
Typical FAP is characterized by hundreds to thousands of colorectal adenomatous polyps and by several extra-colonic manifestations; an attenuated form of polyposis (AFAP), presenting less than 100 adenomas and later onset, has been reported.
Identification of an APC Variant in a Patient with Clinical Attenuated Familial Adenomatous Polyposis.
Gagliano et al., Honolulu, United States. In Case Report Med, 2013
The objective of this case report is to discuss an unclassified germline variant of the adenomatous polyposis coli (APC) gene identified in an older patient with attenuated familial adenomatous polyposis syndrome (AFAP).
A Novel Germline Mutation in Exon 15 of the APC Gene in Attenuated Familial Adenomatous Polyposis: A Report of Two Cases.
Park et al., Seoul, South Korea. In Gut Liver, 2013
Attenuated familial adenomatous polyposis (AFAP) is a variant of familial adenomatous polyposis with fewer than one hundred colorectal polyps and a later age of onset of the cancer.
Mutational spectrum of the APC and MUTYH genes and genotype-phenotype correlations in Brazilian FAP, AFAP, and MAP patients.
Carraro et al., São Paulo, Brazil. In Orphanet J Rare Dis, 2012
APC-mutated patients present classic or attenuated familial adenomatous polyposis (FAP/AFAP), while patients carrying biallelic MUTYH mutations exhibit MUTYH-associated polyposis (MAP).
The genetics of familial adenomatous polyposis (FAP) and MutYH-associated polyposis (MAP).
Kartheuser et al., Brussels, Belgium. In Acta Gastroenterol Belg, 2011
Attenuated FAP (AFAP) is a less severe form of FAP, marked by the presence of < 100 polyps and a later onset of colorectal cancer (CRC).
Tks5 recruits AFAP-110, p190RhoGAP, and cortactin for podosome formation.
Gimona et al., Chieti, Italy. In Exp Cell Res, 2009
Results demonstrate that Tks5 plays a central role in the recruitment of AFAP-110, p190RhoGAP, and cortactin to drive podosome formation.
AFAP120 regulates actin organization during neuronal differentiation.
Lanier et al., Minneapolis, United States. In Differentiation, 2009
These results indicate that AFAP120 plays a role in organizing dynamic actin structures during neuronal differentiation and suggest that AFAP120 may help regulate the transition from motile precursor to morphologically differentiated neurons.
Familial adenomatous polyposis.
Rozen et al., Kefar Sava, Israel. In Orphanet J Rare Dis, 2008
A less aggressive variant of FAP, attenuated FAP (AFAP), is characterized by fewer colorectal adenomatous polyps (usually 10 to 100), later age of adenoma appearance and a lower cancer risk.
The actin cross-linking protein AFAP120 regulates axon elongation in a tyrosine phosphorylation-dependent manner.
Lanier et al., Minneapolis, United States. In Neurosci Lett, 2008
AFAP120 may coordinate Src signaling with the dynamic changes in the actin cytoskeleton that drive growth cone motility and axon elongation.
Phosphorylation of AFAP-110 affects podosome lifespan in A7r5 cells.
Flynn et al., Morgantown, United States. In J Cell Sci, 2008
AFAP-110 phosphorylation and/or dephosphorylation is involved in the regulation of podosome stability and lifespan.
AFAP-110 is required for actin stress fiber formation and cell adhesion in MDA-MB-231 breast cancer cells.
Flynn et al., Morgantown, United States. In J Cell Physiol, 2007
AFAP-110 is required for actin stress fiber formation and cell adhesion in MDA-MB 231 breast cancer cells.
Colonic polyps in children and adolescents.
Durno, Toronto, Canada. In Can J Gastroenterol, 2007
Attenuated familial adenamatous polyposis (AFAP) can occur either by a mutation at the extreme ends of the adenomatous polyposis coli gene or by biallelic mutations in the mutY homologue (MYH) gene.
Correlations between mutation site in APC and phenotype of familial adenomatous polyposis (FAP): a review of the literature.
Vasen et al., Leiden, Netherlands. In Crit Rev Oncol Hematol, 2007
Attenuated FAP (AFAP, <100 colorectal adenomas) is correlated with mutations before codon 157, after codon 1595 and in the alternatively spliced region of exon 9. Severe polyposis (>1000 adenomas) is found in patients with mutations between codons 1250 and 1464.
Matrix-degrading podosomes in smooth muscle cells.
Gimona et al., Salzburg, Austria. In Eur J Cell Biol, 2006
The molecular basis for this local inhibition of contractility includes the clustering of cortactin during podosome formation (which precedes the rapid, local dispersion of myosin, tropomyosin and h1 calponin), and the specific recruitment of 110-kDa actin filament-associated protein (AFAP-110) and 190-kDa Rho-specific GTPase-activating protein (p190RhoGAP) to the microdomains.
Adenomatous polyposis families that screen APC mutation-negative by conventional methods are genetically heterogeneous.
Peltomäki et al., Helsinki, Finland. In J Clin Oncol, 2005
PURPOSE: One third of families with classical adenomatous polyposis (FAP), and a majority of those with attenuated FAP (AFAP), remain APC mutation-negative by conventional methods.
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