Upregulation of keratinocyte lipid binding protein (KLBP) in fat cells of adipocyte lipid binding protein (aP2) knockout mice

N. Rifaarik Coe, M. Simpson, P. A. Bernlohr

Research output: Contribution to journalArticle


KLBP (Mal-1) has previously been localized in keratinocytes, skin cell carcinomas and lens epithelium whereas ALBP (aP2) is exclusively expressed in adipose tissue- Ligand binding analyses of KLBP and ALBP revealed that both proteins bound long chain fatty acids (C18-CZO) with nK Kj values and short chain fatty acids (C10-C16) with uM KJ values. Western analysis of adipose tissue protein (50ug) isolated from wild type, heterozygous ALBP, and knockout ALBP mice revealed no detectable KLBP protein in wild type, 30 ng of KLBP in hétérozygotes, and nearly 60 ng of KLBP protein in the ALBP knockouts. As expected, mRNA for KLBP in adipose tissue of wild type mice was nearly undetectable whereas the mRNA level for KLBP in the ALBP knockouts was 40 fold greater than that measured in adipose tissue of wild type mice. Northern analysis revealed a 50% decrease in ALBP mRNA in hétérozygotes when compared to wild type mice. SDS-PAGE analysis of total fat protein demonstrated a maintained level of lipid binding proteins from all three genotypes. These data clearly show a compensatory upregulation of KLBP in the ALBP knockout mice. Analysis of the fatty acid levels in adipose tissue of normal and ALBP knockout mice have revealed differences in 1 ipid composition, particularly in polyunsaturated fatty acids. This work supported by NSF DMB 9506088.

Original languageEnglish (US)
Pages (from-to)A1379
JournalFASEB Journal
Issue number6
StatePublished - Dec 1 1996


ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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