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May control cell migration by relaying extracellular chemotactic signals to the microtubule cytoskeleton. Additionally we are shipping MEMO1 Antibodies (45) and MEMO1 Proteins (10) and many more products for this protein.
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Study identify Memo as an important key mediator between the heregulin and estrogen signaling pathways, which affects both breast cancer cell migration and proliferation.
HRG/HER2/HER3 signaling promotes AhR-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) in cellular structures involved in migration.
Mediator of ERBB2-driven cell motility (MEMO) promotes extranuclear estrogen receptor signaling involving the growth factor receptors IGF1R and ERBB2.
MEMO1 is involved in breast carcinogenesis via regulating insulin-like growth factor-I receptor-dependent signaling events.
data suggest that Memo controls cell migration by relaying extracellular chemotactic signals to the microtubule cytoskeleton [Memo]
2.1A crystal structure and homology to class III nonheme iron-dependent dioxygenases
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, ErbB2 and PLCgamma1.
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 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