sad / Cyp315a1 antibody

Principal name

sad / Cyp315a1 antibody

Alternative names for sad / Cyp315a1 antibody

CYPCCCXVA1, Protein shadow, Cytochrome P450 315a1 mitochondrial

SwissProt ID

Q9VGH1 (Drome)

Gene ID

44858 (sad)

Ncbi ID

7227, NP_650123

Available reactivities

Dros (Drosophila)

Available hosts


Available applications

Immunocytochemistry/Immunofluorescence (ICC/IF), Immunoprecipitation (IP), Western blot / Immunoblot (WB)

Background of sad / Cyp315a1 antibody

Fruit fly (Drosophila melanogaster) ovaries contains two set of germline stem cells surrounded by a group of highly differentiated somatic cells that express genes for two phenotypes (hedgehog & wingless). The TGF beta super family member, decpentaplegic (dpp) or its homologue BMP2/4 is specifically required for maintenance and promote its cell division in the female germline (1, 2). The Signaling by TGF beta-related factors requires ligand-induced association between type I and type II transmembrane receptors that have endogenous serine/threonine kinases activity. Steroid hormones play an important role in the reproduction, development and homeostasis between transitions between various stages of development (1). In D melonogaster the hormone ecdysone (E) is converted to 20-hydroxyacdysone by a P450 enzyme in peripheral target tissue. The genomic and regulatory effect of this hormone are mediated by activation of a nuclear hormone receptor an activation of transcriptional cascade (2). Recently it has been shown that a product of the Disemboided locus as being potentially involved in the production control of ecdysteroid as a member of the cytochrme P450 family monooxygenese (CYP302A). Mutation in the Disemboided protein result in a number of distinct phenotypes in D. melonogaster including disruption in dorsal closure, head evolution, gut morphogenesis, and failure to produce embryonic cuticle. Most of these disruptions are the result of low affinity of 20E to its receptor due to significant reduction in the expression of IMP-E1 gene. Several other mutations in the “Halloween” group of proteins, including Shadow (sad) also resulted in similar phenotypes (3, 4). The co-expression of dib and sad causes increased metabolism of ketotriol to ecdyson (2) and the two proteins are concentrated with in the individual segment (2).

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