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Delta-aminolevulinic acid dehydratase assay.
TLDR
The enzyme activity in adult male rat liver was 2.22 and 1.94 mumol PBG formed/g liver/h for homogenates assayed with or without dithiothreitol, respectively.
The porphyrias.
  • S. Sassa
  • Medicine
    Photodermatology, photoimmunology & photomedicine
  • 3 October 2018
Heme mediates derepression of Maf recognition element through direct binding to transcription repressor Bach1
TLDR
It is shown that heme binds specifically to Bach1 and regulates its DNA‐binding activity, suggesting that increased levels of heme inactivate the repressor Bach1, resulting in induction of a host of genes with MAREs.
Identification of a Human Heme Exporter that Is Essential for Erythropoiesis
TLDR
It is demonstrated that human FLVCR exports cytoplasmic heme and hypothesize that humanFLVCR is required on developing erythroid cells to protect them from heme toxicity, the first description of a mammalian heme transporter.
Modern diagnosis and management of the porphyrias
  • S. Sassa
  • Medicine
    British journal of haematology
  • 1 November 2006
TLDR
For the diagnosis of clinically expressed porphyrias, a logical stepwise approach including the analysis of porphyrins and their precursors should not be underestimated, as it is still very useful, and is often the best from the cost‐effective point of view.
Lead Binding to δ-Aminolevulinic Acid Dehydratase (ALAD) in Human Erythrocytes
Over 99% of the lead present in blood is usually found in erythrocytes. To investigate the nature of this selective accumulation of lead in erythrocytes, the specific binding of lead to proteins in
Establishment and characterization of an erythropoietin-dependent subline, UT-7/Epo, derived from human leukemia cell line, UT-7.
TLDR
UT-7/Epo cells had progressed further in erythroid development than UT-7 cells, and it was suggested that long-term culture in Epo had promoted this differentiation.
Molecular aspects of the inherited porphyrias
TLDR
Molecular aspects of the inherited porphyrias and their role in infectious disease are studied.
Why heme needs to be degraded to iron, biliverdin IXalpha, and carbon monoxide?
  • S. Sassa
  • Medicine
    Antioxidants & redox signaling
  • 2004
TLDR
The breakdown of heme to smaller elements has its own significance in essential cellular metabolism, and HO is one of the major players in these mechanisms, and it catabolizes free he me to iron, biliverdin IXalpha, and carbon monoxide.
Heme oxygenase-1: a novel therapeutic target in oxidative tissue injuries.
TLDR
Recent advances in the regulatory mechanism of ho-1 gene expression and the role of HO-1 in various models of experimental oxidative tissue injuries, and its potential therapeutic implications are reviewed.
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