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anti-Human DBN1 Antibodies:
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Cow (Bovine) Monoclonal DBN1 Primary Antibody for ICC, IF - ABIN151450
Kojima, Kato, Shirao, Obata: Nucleotide sequences of two embryonic drebrins, developmentally regulated brain proteins, and developmental change in their mRNAs. in Brain research 1989
Show all 6 Pubmed References
Human Polyclonal DBN1 Primary Antibody for IHC (fro), IF - ABIN285747
Ganong, Kramer, Salmon, Reid, Lovinger, Scapagnini, Boryczka, Shackelford: Pharmacological evidence for inhibition of ACTH secretion by a central adrenergic system in the dog. in Neuroscience 2001
Human Monoclonal DBN1 Primary Antibody for FACS, WB - ABIN1558085
Hayashi, Ishikawa, Kawai-Hirai, Takagi, Taketomi, Shirao: Domain analysis of the actin-binding and actin-remodeling activities of drebrin. in Experimental cell research 2000
Show all 5 Pubmed References
Drebrin may regulate activities of epigenetic reader ZMYND8 (show ZMYND8 Antibodies) via its cytoplasmic sequestration.
Inhibition of cortactin (show CTTN Antibodies) or dynamin-2 (show DNM2 Antibodies) abrogated the increased virus entry observed in DBN1-deficient cells, suggesting that DBN1 suppresses dynamin (show DNM1 Antibodies)-mediated endocytosis via interaction with cortactin (show CTTN Antibodies).
Lack of drebrin leads to the dysfunction of cell-cell communication, resulting in aberrant migration of metastatic cancer cells, aberrant synaptic function in dementia, and rupture of endothelial integrity.
One candidate pathway coupling actin filaments to microtubules consists of the actin filament-binding protein drebrin and the microtubule-binding +TIP protein EB3 (show MAPRE3 Antibodies). This pathway is regulated proximally by cyclin-dependent kinase 5 (show CDK5 Antibodies) phosphorylation of drebrin but the upstream elements in the pathway have yet to be identified.
These observations indicate that drebrin loss in dendritic spines occurs at the prodromal stage of Alzheimer's disease (AD), before the density and morphology of dendritic spines change. Quantitation of drebrin may be a possible tool for diagnosing the prodromal stage of AD, before dementia development in AD.
Taking into account that connexin-43 (Cx43 (show GJA1 Antibodies)) (together with Cx30 (show GJB6 Antibodies)) is heavily expressed in astrocytes and that drebrin supports cell-cell contacts, the understanding of details of how brain cells live and die reveals molecular pathology involved in neurodegeneration, Alzheimer's disease (AD), other cognitive disorders, and aging
further studies on drebrin and its binding proteins will be of great importance to elucidate the pathologies of various diseases and may contribute to their medical treatment and diagnostics development.
through its interaction with CXCR4 (show CXCR4 Antibodies) and the actin cytoskeleton, drebrin regulates T cell activation. CD4 (show CD4 Antibodies)(+) T cells are one of the main targets for the human immunodeficiency virus (HIV)-1.
Our work has shown that the immunosuppressant compound BTP2, which blocks Ca(2 (show CA2 Antibodies)+) influx into cells, interacts with the actin-reorganizing protein, drebrin. Here we review the role of drebrin in the regulation of calcium signaling, with a focus on immune cells.
Upregulation of drebrin was noted in several types of cancers, e.g., basal cell carcinomas for which it may serve as marker, liver metastases of colon carcinomas, and bladder cancer, suggesting that it is involved in regulating actin dynamics during tumor development, progression, and metastasis.
Hippocampal Drebrin protein (show DBNL Antibodies) expression levels in adult APP (show APP Antibodies)/PS1 (show PSEN1 Antibodies) mice decline with age. Behavioral data demonstrated that cognitive and probe activities decline with age. A correlation analysis showed that the expression level of the Drebrin protein (show DBNL Antibodies) significantly correlatives with behavioral performance in Alzheimer's disease mice.
In subventricular zone of Dbn1-null mice number of neuroblasts and cell proliferation decreased, although cell death remained unchanged.
Drebrin A is highly enriched in dendritic spines, but its effects on actin morphology, dynamics, and interplay with other actin regulators are yet to be clarified. Here we review recent advances in understanding drebrin effects on actin morphology and dynamics.
Drebrin A can be found co-clustering with NR2B (show GRIN2B Antibodies)-containing NMDARs at the plasma membrane, while NR2A (show GRIN2A Antibodies)-containing NMDARs co-traffic into the spine cytoplasm but do not co-cluster at the plasma membrane.
these findings suggest that during cell migration drebrin is involved in retraction processes but not in lamellipodia formation. The novel, sizable juxtanuclear drebrin-enriched zone remains to be characterized in detail with respect to its molecular assembly and functions.
bn1 (show CCR6 Antibodies) expression is induced during myoblast differentiation, in a p38 MAP kinase (show MAPK14 Antibodies)- and MyoD (show MYOD1 Antibodies)- dependent manner. RNAi-mediated depletion of drebrin, or treatment with a chemical drebrin inhibitor, resulted in a similar phenotype in myoblasts: defective differentiation, with low levels of early and late differentiation markers and inefficient production of myofibers.
Study determines the specific roles of drebrin in the regulation of the axonal cytoskeleton, and provides evidence that drebrin contributes to the coordination of the actin and microtubule cytoskeleton during the initial stages of axon branching.
Drebrin reduces SMC (show DYM Antibodies) activation through its interaction with the actin cytoskeleton but independently of its interaction with Homer (show HOMER1 Antibodies) scaffolds to prevent neointima formation.
Data suggest further studies to elucidate the effect of drebrin (Dbn) on the development and progression of Alzheimer's disease (AD).
The protein encoded by this gene is a cytoplasmic actin-binding protein thought to play a role in the process of neuronal growth. It is a member of the drebrin family of proteins that are developmentally regulated in the brain. A decrease in the amount of this protein in the brain has been implicated as a possible contributing factor in the pathogenesis of memory disturbance in Alzheimer's disease. At least two alternative splice variants encoding different protein isoforms have been described for this gene.
developmentally-regulated brain protein
, drebrin E
, drebrin E2
, drebrin A
, developmentally regulated brain protein
, drebrin 1