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LIMA1 encodes a cytoskeleton-associated protein that inhibits actin filament depolymerization and cross-links filaments in bundles. Zusätzlich bieten wir Ihnen LIMA1 Proteine (3) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal LIMA1 Primary Antibody für IP, IHC - ABIN250686
Han, Kosako, Watanabe, Hattori: Extracellular signal-regulated kinase/mitogen-activated protein kinase regulates actin organization and cell motility by phosphorylating the actin cross-linking protein EPLIN. in Molecular and cellular biology 2007
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Human Polyclonal LIMA1 Primary Antibody für ICC, IF - ABIN4308788
Stadler, Rexhepaj, Singan, Murphy, Pepperkok, Uhlén, Simpson, Lundberg: Immunofluorescence and fluorescent-protein tagging show high correlation for protein localization in mammalian cells. in Nature methods 2013
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Human Polyclonal LIMA1 Primary Antibody für IP - ABIN250691
Zhang, Wang, Iqbal, Wang, Osunkoya, Chen, Chen, Shin, Yuan, Wang, Zhau, Chung, Ritenour, Kucuk, Wu: Epidermal growth factor promotes protein degradation of epithelial protein lost in neoplasm (EPLIN), a putative metastasis suppressor, during epithelial-mesenchymal transition. in The Journal of biological chemistry 2013
Cow (Bovine) Polyclonal LIMA1 Primary Antibody für WB - ABIN2775866
Maul, Song, Amann, Gerbin, Pollard, Chang: EPLIN regulates actin dynamics by cross-linking and stabilizing filaments. in The Journal of cell biology 2003
Data provide evidence that downregulation of EPLIN-alpha may be associated with poor prognosis for patients with epithelial ovarian cancer (EOC), and that this molecule appears to play a tumour suppressor role by inhibition of EOC growth and migration.
EPLIN is functionally linked to molecules like actin and paxillin (zeige PXN Antikörper) and has been implicated in a number of potential pathways to enhance metastatic potential
a major activity of DNp73 is to establish initiation of the invasion-metastasis cascade via EPLIN-dependent IGF1R (zeige IGF1R Antikörper) regulation
EGF (zeige EGF Antikörper) promotes epithelial-mesenchymal transition and induces degradation of EPLIN, a putative suppressor of prostate cancer metastasis.
Together with the findings that EPLIN-alpha inhibits cellular growth and invasion, we conclude that EPLIN-alpha is a tumour suppressor of oesophageal cancer
EPLIN clutch is necessary for stabilization of capillary structures in an angiogenesis model.
EPLIN downregulation promotes epithelial-mesenchymal transition in prostate cancer cells and correlates with clinical lymph node metastasis.
EPLIN functions to link the cadherin-catenin complex to F-actin and simultaneously stabilizes this population of actin fibers, resulting in the establishment of the adhesion
expression of EPLIN-alpha in breast cancer is down-regulated in breast cancer cells .
EPLIN protein may function during cytokinesis to maintain local accumulation of key cytokinesis proteins at the furrow.
findings suggest that PINCH-1 (zeige LIMS1 Antikörper) regulates integrin-mediated adhesion of keratinocytes through the interactions with ILK (zeige ILK Antikörper) as well as EPLIN.
Eplin-alpha transcription is regulated by actin-MAL-SRF signalling.
EPLIN may function in growth control by associating with and regulating the actin cytoskeleton
ERK-mediated phosphorylation of EPLIN contributes to actin filament reorganization and enhanced cell motility.
This gene encodes a cytoskeleton-associated protein that inhibits actin filament depolymerization and cross-links filaments in bundles. It is downregulated in some cancer cell lines. Alternatively spliced transcript variants encoding different isoforms have been described for this gene, and expression of some of the variants maybe independently regulated.
LIM domain and actin-binding protein 1
, epithelial protein lost in neoplasm
, LIM domain and actin binding 1
, epithelial protein lost in neoplasm beta
, sterol regulatory element binding protein 3
, epithelial protein lost in neoplasm-a
, epithelial protein lost in neoplasm-b