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Monoclonal Antibody Western Blotting Female Genitalia Development

Also showing Monoclonal Antibody Immunoprecipitation Female Genitalia Morphogenesis, Monoclonal Antibody Immunoprecipitation Female Genitalia Development, Monoclonal Antibody Western Blotting Female Genitalia Morphogenesis

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse

Application Methods: Immunoprecipitation, Western Blotting

Background: CHD7 belongs to the chromodomain helicase DNA-binding (CHD) family of ATP-dependent chromatin remodeling proteins (1). The CHD family of proteins has been shown to play an important role in regulating gene expression by altering the chromatin structure at target genes (1,2). The nine members of the CHD family are characterized by the presence of two tandem chromodomains in the N-terminal region and an SNF2-like ATPase domain near the central region of the protein (2-4). The CHD proteins can be further divided into three subgroups based on the presence of additional conserved functional domains. CHD7 belongs to the third subgroup of CHD proteins together with CHD6, 8, and 9, which are distinguished by the presence of three conserved region (CR) domains, a switching-defective protein 3, adaptor 2, nuclear receptor co-repressor, transcription factor IIB (SANT) like domain, two brahma and kismet (BRK) domains, and a DNA binding domain (2). CHD7 regulates embryonic stem cell (ESC) specific gene expression together with ESC master regulators Oct-4, Sox2 and nanog, and is necessary for neural stem cell development and formation of the neural crest (5-7). Research studies have shown that CHD7 mutations are frequently found in patients with CHARGE syndrome (coloboma of the eye, heart defects, atresia of the choanae, retardation of growth/development, genital/urinary abnormalities, and ear abnormalities and deafness) (8).

$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).

$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).