Human Protocadherin gamma C3 Alexa Fluor® 647-conjugated Antibody
Human Protocadherin gamma C3 Alexa Fluor® 647-conjugated Antibody Summary
Accession # Q9UN70
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Detection of Protocadherin gamma C3 in HEK293 Human Cell Line Transfected with Human Protocadherin gamma C3 by Flow Cytometry. HEK293 human embryonic kidney cell line transfected with human Protocadherin gamma C3 was stained with Mouse Anti-Human Protocadherin gamma C3 Alexa Fluor® 647‑conjugated Monoclonal Antibody (Catalog # FAB83641R, filled histogram) or isotype control antibody (Catalog # IC002R, open histogram). View our protocol for Staining Membrane-associated Proteins.
Preparation and Storage
- 12 months from date of receipt, 2 to 8 °C as supplied.
Background: Protocadherin gamma C3
Protocadherin gamma C3 is a member of the gamma subgroup of clustered protocadherins (1). Like other gamma protocadherins, mature Protocadherin gamma C3 contains six extracellular cadherin domains, a transmembrane region, and a cytoplasmic domain (2, 3). Within the ECD, human Protocadherin gamma C3 shares 91% and 92% amino acid sequence identity with mouse and rat Protocadherin gamma C3, respectively. It plays an important role in cell adhesion and cell recognition through Ca2+ -dependent homophilic interaction (4). MMP-mediated shedding of gamma protocadherins and release of their cytoplasmic domain by the gamma -secretase complex results in translocation of the intracellular domain into the nucleus and transcriptional activation of target genes (5-7). Protocadherin gamma C3 is cleaved within its ectodomain by ADAM10 in fibroblasts and neuronal cells (8). Deletion of the entire protocadherin gamma gene cluster is embryonic lethal in mice (9). Protocadherin gamma C3 is most notably expressed in the nervous system (10). Conditional deletion of the protocadherin gamma gene cluster in mice affects development of retinal ganglion cells and spinal cord interneurons, resulting in decreased synapses and increased neuronal apoptosis (9, 11-14). The C-type protocadherin gamma isoforms specifically may be responsible for the increased apoptosis observed in mice lacking the entire protocadherin gamma gene cluster (15). Cortical neuron-specific deletion of the protocadherin gamma gene cluster results in dendritic arborization defects (16). The protocadherin gamma subfamily may also be involved in cerebrospinal fluid production and the maturation and differentiation of postnatally generated olfactory granule cells (17, 18).
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