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Human Establishment of Planar Polarity

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey

Application Methods: Immunoprecipitation, Western Blotting

Background: Frizzled (Fzd) belongs to the seven transmembrane-spanning G-protein-coupled receptor (GPCR) superfamily (1). Fzds have a large extracellular N-terminal region containing a cysteine-rich domain (CRD), which is involved in binding to Wnt proteins (1,2). The intracellular C-terminus binds to the PDZ domain of Dvl proteins, a major signaling component downstream of Fzd (3). Wnt proteins bind to Fzd and the co-receptors LRP5 or LPR6, and activate Wnt/β-catenin pathway through inhibiting phosphorylation of β-catenin by GSK3-β (4,5). In addition to this canonical Wnt/β-catenin pathway, some Wnt proteins can also activate the Fzd/Ca2+ pathway and Fzd/PCP (planar cell polarity) pathway (6,7). The mammalian Fzd subfamily has 10 members (Fzd1 to Fzd10) and they may mediate signaling through different pathways (8). Some Fzds can also bind to other secreted proteins, like Norrin and R-Spondin (9-11).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: PTK7 (CCK4) is a non-active receptor tyrosine kinase originally identified in colon carcinoma cells (1). PTK7 functions in cell adhesion, cell migration, cell polarity, proliferation, actin cytoskeleton reorganization, and apoptosis to regulate embryogenesis, epithelial tissue organization, neuronal tube closure, neuronal crest formation, and axon guidance (2-5). PTK7 acts as a co-receptor in both the non-canonical (also known as the Wnt/planar cell polarity signaling) and the canonical Wnt signaling pathways (6). In the non-canonical Wnt pathway, PTK7 activates downstream signaling by direct interaction with RACK1 and recruitment of DSH into the membrane localized receptor complex (3,6,7). PTK7 exerts an inhibitory effect on canonical Wnt pathway signal transduction through competition for frizzled receptor binding at the membrane surface (8). PTK7 gene expression is regulated by Cdx (9), while protein stability is regulated by membrane associated proteinase degradation. PTK7 is targeted for proteolytic degradation and extracellular domain shedding by the metalloproteinases MMP14 and Adam17, leading to enhanced cell proliferatiion, migration, and facilitated cancer cell invasion (10,11). PTK7 has been shown to regulate other signaling pathways by functioning as a co-receptor with membrane receptors, such as Plexin A1 and VEGFR1 (12-14).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: Synapse-associated protein 102 (SAP102, DLG3) belongs to the membrane-associated guanylate kinase (MAGUK) protein family and is a homolog of the Drosophila disc large (dlg) tumor suppressor protein. SAP102 consists of three PDZ domains, a Src homology 3 (SH3) domain, and a guanylate kinase (GK) domain (1). The SAP102 protein is more highly expressed in nonproliferating cells than in proliferating cells, indicating a role in the negative regulation of cell growth. SAP102 interacts with the carboxy terminus of the adenomatous polyposis coli (APC) tumor suppressor protein. Furthermore, SAP102 associates with PSD95 in the presence of calcium while the SH3 domain of SAP102 binds calmodulin (2,3). All three PDZ domains of SAP102 participate in binding to the NMDA receptor, interacting specifically with the carboxy-terminal domain of the N-methyl-D-aspartate receptor 2B (NR2B). This SAP102-NR2B interaction may facilitate AMPA receptor withdrawal from the postsynaptic membrane by inhibiting the Erk/MAPK pathway (1,4). Neuronal SAP102 is concentrated at dendritic shafts and spines, axons, and synaptic junctions. At excitatory synapses, SAP102 is involved in NMDA receptor clustering and immobilization and links NMDA receptors to the submembraneous cytomatrix (4). SAP102 and the NMDA receptor function together to mediate plasticity, behavior, and signal transduction (1). A nonsyndromic form of X-linked mental retardation is caused by loss-of-function mutations to the SAP102 gene. The SAP102 protein may be involved in autism since MAGUK proteins in the NMDA receptor complex bind directly to the autism susceptibility gene, neuroligin (1,5).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Immunofluorescence (Immunocytochemistry), Western Blotting

Background: The p53 tumor suppressor protein plays a major role in cellular response to DNA damage and other genomic aberrations. Activation of p53 can lead to either cell cycle arrest and DNA repair or apoptosis (1). In addition to p53, mammalian cells contain two p53 family members, p63 and p73, which are similar to p53 in both structure and function (2). While p63 can induce p53-responsive genes and apoptosis, mutation of p63 rarely results in tumors (2). Research investigators frequently observe amplification of the p63 gene in squamous cell carcinomas of the lung, head and neck (2,3). The p63 gene contains an alternative transcription initiation site that yields a truncated ΔNp63 lacking the transactivation domain, and alternative splicing at the carboxy-terminus yields the α, β, and γ isoforms (3,4).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Chromatin IP, Immunofluorescence (Immunocytochemistry), Immunoprecipitation, Western Blotting

Background: The p53 tumor suppressor protein plays a major role in cellular response to DNA damage and other genomic aberrations. Activation of p53 can lead to either cell cycle arrest and DNA repair or apoptosis (1). In addition to p53, mammalian cells contain two p53 family members, p63 and p73, which are similar to p53 in both structure and function (2). While p63 can induce p53-responsive genes and apoptosis, mutation of p63 rarely results in tumors (2). Research investigators frequently observe amplification of the p63 gene in squamous cell carcinomas of the lung, head and neck (2,3). The p63 gene contains an alternative transcription initiation site that yields a truncated ΔNp63 lacking the transactivation domain, and alternative splicing at the carboxy-terminus yields the α, β, and γ isoforms (3,4).

$303
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Flow Cytometry, Immunohistochemistry (Paraffin), Western Blotting

Background: The p53 tumor suppressor protein plays a major role in cellular response to DNA damage and other genomic aberrations. Activation of p53 can lead to either cell cycle arrest and DNA repair or apoptosis (1). In addition to p53, mammalian cells contain two p53 family members, p63 and p73, which are similar to p53 in both structure and function (2). While p63 can induce p53-responsive genes and apoptosis, mutation of p63 rarely results in tumors (2). Research investigators frequently observe amplification of the p63 gene in squamous cell carcinomas of the lung, head and neck (2,3). The p63 gene contains an alternative transcription initiation site that yields a truncated ΔNp63 lacking the transactivation domain, and alternative splicing at the carboxy-terminus yields the α, β, and γ isoforms (3,4).

$122
20 µl
$293
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Chromatin IP, Chromatin IP-seq, Flow Cytometry, Immunofluorescence (Immunocytochemistry), Immunoprecipitation, Western Blotting

Background: The p53 tumor suppressor protein plays a major role in cellular response to DNA damage and other genomic aberrations. Activation of p53 can lead to either cell cycle arrest and DNA repair or apoptosis (1). In addition to p53, mammalian cells contain two p53 family members, p63 and p73, which are similar to p53 in both structure and function (2). While p63 can induce p53-responsive genes and apoptosis, mutation of p63 rarely results in tumors (2). Research investigators frequently observe amplification of the p63 gene in squamous cell carcinomas of the lung, head and neck (2,3). The p63 gene contains an alternative transcription initiation site that yields a truncated ΔNp63 lacking the transactivation domain, and alternative splicing at the carboxy-terminus yields the α, β, and γ isoforms (3,4).

$303
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Immunohistochemistry (Paraffin), Immunoprecipitation, Western Blotting

Background: The p53 tumor suppressor protein plays a major role in cellular response to DNA damage and other genomic aberrations. Activation of p53 can lead to either cell cycle arrest and DNA repair or apoptosis (1). In addition to p53, mammalian cells contain two p53 family members, p63 and p73, which are similar to p53 in both structure and function (2). While p63 can induce p53-responsive genes and apoptosis, mutation of p63 rarely results in tumors (2). Research investigators frequently observe amplification of the p63 gene in squamous cell carcinomas of the lung, head and neck (2,3). The p63 gene contains an alternative transcription initiation site that yields a truncated ΔNp63 lacking the transactivation domain, and alternative splicing at the carboxy-terminus yields the α, β, and γ isoforms (3,4).

$348
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to phycoerythrin (PE) and tested in-house for direct flow cytometry analysis in human cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated p63-α (D2K8X) XP® Rabbit mAb #13109.
APPLICATIONS
REACTIVITY
Human

Application Methods: Flow Cytometry

Background: The p53 tumor suppressor protein plays a major role in cellular response to DNA damage and other genomic aberrations. Activation of p53 can lead to either cell cycle arrest and DNA repair or apoptosis (1). In addition to p53, mammalian cells contain two p53 family members, p63 and p73, which are similar to p53 in both structure and function (2). While p63 can induce p53-responsive genes and apoptosis, mutation of p63 rarely results in tumors (2). Research investigators frequently observe amplification of the p63 gene in squamous cell carcinomas of the lung, head and neck (2,3). The p63 gene contains an alternative transcription initiation site that yields a truncated ΔNp63 lacking the transactivation domain, and alternative splicing at the carboxy-terminus yields the α, β, and γ isoforms (3,4).

$111
20 µl
$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Western Blotting

Background: The Wnt family includes several secreted glycoproteins that play important roles in animal development (1). There are 19 Wnt genes in the human genome that encode functionally distinct Wnt proteins (2). Wnt members bind to the Frizzled family of seven-pass transmembrane proteins and activate several signaling pathways (3). The canonical Wnt/β-catenin pathway also requires a coreceptor from the low-density lipoprotein receptor family (4). Aberrant activation of Wnt signaling pathways is involved in several types of cancers (5).

$111
20 µl
$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey, Mouse, Rat

Application Methods: Western Blotting

Background: Rac and Cdc42 are members of the Rho-GTPase family. In mammals, Rac exists as three isoforms, Rac1, Rac2 and Rac3, which are highly similar in sequence. Rac1 and Cdc42, the most widely studied of this group, are ubiquitously expressed. Rac2 is expressed in cells of hematopoietic origin, and Rac3, while highly expressed in brain, is also found in many other tissues. Rac and Cdc42 play key signaling roles in cytoskeletal reorganization, membrane trafficking, transcriptional regulation, cell growth and development (1). GTP binding stimulates the activity of Rac/Cdc42, and the hydrolysis of GTP to GDP through the protein's intrinsic GTPase activity, rendering it inactive. GTP hydrolysis is aided by GTPase activating proteins (GAPs), while exchange of GDP for GTP is facilitated by guanine nucleotide exchange factors (GEFs). Another level of regulation is achieved through the binding of RhoGDI, a guanine nucleotide dissociation inhibitor, which retains Rho family GTPases, including Rac and Cdc42, in their inactive GDP-bound state (2,3).

$122
20 µl
$303
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Western Blotting

Background: Rac and Cdc42 are members of the Rho-GTPase family. In mammals, Rac exists as three isoforms, Rac1, Rac2 and Rac3, which are highly similar in sequence. Rac1 and Cdc42, the most widely studied of this group, are ubiquitously expressed. Rac2 is expressed in cells of hematopoietic origin, and Rac3, while highly expressed in brain, is also found in many other tissues. Rac and Cdc42 play key signaling roles in cytoskeletal reorganization, membrane trafficking, transcriptional regulation, cell growth and development (1). GTP binding stimulates the activity of Rac/Cdc42, and the hydrolysis of GTP to GDP through the protein's intrinsic GTPase activity, rendering it inactive. GTP hydrolysis is aided by GTPase activating proteins (GAPs), while exchange of GDP for GTP is facilitated by guanine nucleotide exchange factors (GEFs). Another level of regulation is achieved through the binding of RhoGDI, a guanine nucleotide dissociation inhibitor, which retains Rho family GTPases, including Rac and Cdc42, in their inactive GDP-bound state (2,3).