APAF1 Antibodies

APAF1 (Apoptotic Peptidase Activating Factor 1) is a Protein Coding gene. Diseases associated with APAF1 include Dystrophinopathies and Retinal Ischemia. Among its related pathways are Direct p53 effectors and Innate Immune System. Gene Ontology (GO) annotations related to this gene include identical protein binding and ADP binding.

CUSABIO produces high-quality anti-APAF1 antibodies (includes polyclonal antibodies, monoclonal antibodies, recombinant antibodies) in house with strict quality control. And they can help you discover more in your research.
These APAF1 antibodies are validated in multiple tissues with various applications and covering a broad range of life science research and drug development. They are featured with high specificity, multiple epitopes recognition, and wide species reactivity. Moreover, CUSABIO provides various options on sizes, excellent technical support and APAF1 antibodies custom service.

APAF1 Antibodies Catalog

APAF1 Antibodies for Homo sapiens (Human)

APAF1 Antibodies for Danio rerio (Zebrafish) (Brachydanio rerio)

APAF1 Background

Apoptotic protease-activating factor 1 (APAF1) is a cytoplasmic protein in humans that is encoded by the APAF1 gene. APAF1 is a multi-domain adapter protein containing a caspase recruitment domain (CARD), followed by a nucleotide-binding & oligomerization domain, a short helical motif, and several copies of the WD40 repeat domain [1][2][3]. ATPase domain of APAF1 is homologous to CED-4 in Caenorhabditis elegans. APAF1 normally presents an inactive monomer with locked conformation bound to dATP or ATPT [4]. During the intrinsic or mitochondrial pathway of apoptosis, APAF1 oligomerizes in the presence of dATP in response to cytochrome c release and recruits procaspase-9 & caspase-3 to form apoptosome, eventually leading to apoptosis. APAF1 is, therefore, a crucial player in development due to its mediation of the mitochondria-dependent apoptosis. Although no alterations were observed in heterozygous mice, APAF1 deficient embryos died between embryonic day 16 and postnatal day 0 [5]. Abnormal Apaf-/- embryos were found at embryonic day 11.5, and later they showed alterations of the development of many organs [5]. The hypomorphic allele of APAF1 has reported causing reduced levels of the normal APAF1 transcript, thus affecting the neural tube development and fog (forebrain overgrowth) [6][7]. Results showed that either the absence of APAF1 or downregulation of APAF1 (below 50%) is deleterious for the development causing milder effects compatible with life and with possible links to human diseases [8]. Moreover, Soengas and his coworkers found that APAF1 or caspase-9 inactivation substitutes p53 loss in promoting the oncogenic transformation of myc-expressing cells by analyzed p53-null, Apaf1-null, and caspase-9-null MEFs [9]. Frame-shift mutations in the APAF1 gene were detected at low frequencies (13-15%) in gastrointestinal cancer (microsatellite mutator phenotype) [10].

[1] Zou H, Henzel WJ, et al. Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3 [J]. Cell. Aug 1997, 90 (3): 405–13.
[2] Riedl SJ, Li W, et al. Structure of the apoptotic protease-activating factor 1 bound to ADP [J]. Nature. 2005 Apr 14; 434(7035):926-33.
[3] Yu X, Acehan D, et al. A structure of the human apoptosome at 12.8 A resolution provides insights into this cell death platform [J]. Structure. 2005 Nov; 13(11):1725-35.
[4] Kim HE, Du F, et al. Formation of apoptosome is initiated by cytochrome c-induced dATP hydrolysis and subsequent nucleotide exchange on Apaf-1 [J]. Proc Natl Acad Sci U S A. 2005 Dec 6; 102 (49):17545-50.
[5] Cecconi F., Alvarez-Bolado G., et al. Apaf1 (CED-4 homolog) regulates programmed cell death in mammalian development [J]. Cell., 1998, 94(6): 727-37.
[6] Honarpour N., Gilbert S.L., et al. Apaf-1 deficiency and neural tube closure defects are found in fog mice [J]. Proc. Natl. Acad. Sci. USA, 2001, 98: 9683-9687.
[7] Spellicy CJ, Norris J, et al. Key apoptotic genes APAF1 and CASP9 implicated in recurrent folate-resistant neural tube defects [J]. Eur J Hum Genet. 2018 Mar;26(3):420-427.
[8] Moreno S., Ferraro E., et al. Apaf1 reduced expression levels generate a mutant phenotype in adult brain and skeleton [J]. Cell Death Differ., 2002, 9: 340-342.
[9] Soengas M.S., Alarcon R.M., et al. Apaf-1 and Caspase-9 in p53-dependent apoptosis and tumor inhibition [J]. Science, 1999, 284:156-159.
[10] Yamamoto H., Gil J., et al. Frameshift mutations in Fas, Apaf-1, and Bcl-10 in gastrointestinal cancer of the microsatellite mutator phenotype [J]. Cell Death Differ., 2000, 7: 238-239.

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