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May control cell migration by relaying extracellular chemotactic signals to the microtubule cytoskeleton. Additionally we are shipping MEMO1 Proteins (10) and MEMO1 Kits (8) and many more products for this protein.
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Study identify Memo as an important key mediator between the heregulin (show NRG1 Antibodies) and estrogen signaling pathways, which affects both breast cancer cell migration and proliferation.
HRG (show NRG1 Antibodies)/HER2 (show ERBB2 Antibodies)/HER3 (show ERBB3 Antibodies) signaling promotes AhR (show AHR Antibodies)-mediated Memo-1 expression and migration in colorectal cancer
Biochemical assays revealed that Memo is a copper-dependent redox enzyme that promoted a more oxidized intracellular milieu and stimulated the production of reactive oxygen species (ROS (show ROS1 Antibodies)) in cellular structures involved in migration.
Mediator of ERBB2 (show ERBB2 Antibodies)-driven cell motility (MEMO) promotes extranuclear estrogen receptor (show ESR1 Antibodies) signaling involving the growth factor receptors IGF1R (show IGF1R Antibodies) and ERBB2 (show ERBB2 Antibodies).
MEMO1 is involved in breast carcinogenesis via regulating insulin-like growth factor-I receptor (show IGF1R Antibodies)-dependent signaling events.
data suggest that Memo controls cell migration by relaying extracellular chemotactic signals to the microtubule cytoskeleton [Memo]
Memo-RhoA-mDia1 signaling coordinates the organization of the lamellipodial actin network, adhesion site formation, and microtubule outgrowth within the cell leading edge to sustain cell motility.
Memo was detected in complexes with cofilin (show CFL1 Antibodies), ErbB2 (show ERBB2 Antibodies) and PLCgamma1 (show PLCG1 Antibodies).
Memo1 showed robust expression in the perichondrium and periosteum of the developing cranial base, but only modest expression in the palatal shelves. Neural crest cell-specific deletion of Memo1 caused a failure of anterior cranial base ossification indicating a cell autonomous role for MEMO1 in the development of these structures, but palatal formation was normal, indicating a non-autonomous role in palatal closure.
our results show that Memo has a novel role in the S1P (show S1PR1 Antibodies) pathway and that Memo is needed to promote cell-autonomous S1PR activation.
tissue distribution of Memo in mice.
May control cell migration by relaying extracellular chemotactic signals to the microtubule cytoskeleton. Mediator of ERBB2 signaling. The MEMO1-RHOA-DIAPH1 signaling pathway plays an important role in ERBB2-dependent stabilization of microtubules at the cell cortex. It controls the localization of APC and CLASP2 to the cell membrane, via the regulation of GSK3B activity. In turn, membrane-bound APC allows the localization of the MACF1 to the cell membrane, which is required for microtubule capture and stabilization (By similarity).
, C21orf19-like protein
, protein memo
, mediator of ErbB2-driven cell motility 1
, mediator of cell motility 1
, Methylation modifier for class I HLA
, HCV NS5A-transactivated protein 7
, hepatitis C virus NS5A-transactivated protein 7