PEPT (SLC15A) Family

Sugiura, Tomoko; Umeda, Saki; Tsuji, Akira; Kato, Yukio

doi:10.1002/9781118353240.ch10

Pharmacogenomics of Human Drug Transporters 2013

DOI: 10.1002/9781118353240.ch10

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PEPT (SLC15A) Family

Tomoko Sugiura

Saki Umeda

Akira Tsuji

et al.

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2015

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Cited by 1 publication

(2 citation statements)

References 84 publications

(108 reference statements)

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“…In mammals, the uptake of small peptides by the Slc15A family of oligo/dipeptide transporters provides an effective and energy-saving intracellular source of amino acids 11 12 13 . These transporters are encoded by the Slc15A1 (previously designated Pept1 ), Slc15A2 ( Pept2 ), Slc15A4 ( Pht1 ) and Slc15A3 ( Pht2 ) genes.…”

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confidence: 99%

“…These transporters are encoded by the Slc15A1 (previously designated Pept1 ), Slc15A2 ( Pept2 ), Slc15A4 ( Pht1 ) and Slc15A3 ( Pht2 ) genes. Oligo-/dipeptide uptake dependent on Slc15A1/2 has been well studied in renal and intestinal epithelial cells 11 12 13 , but the functions of these transporters in haematopoietic cells are obscure. We propose that Slc15A2 dipeptide transporter activity sustains CML stem cell maintenance by guaranteeing an alternative nutrient supply.…”

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Dipeptide species regulate p38MAPK–Smad3 signalling to maintain chronic myelogenous leukaemia stem cells

et al. 2015

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Understanding the specific survival of the rare chronic myelogenous leukaemia (CML) stem cell population could provide a target for therapeutics aimed at eradicating these cells. However, little is known about how survival signalling is regulated in CML stem cells. In this study, we survey global metabolic differences between murine normal haematopoietic stem cells (HSCs) and CML stem cells using metabolomics techniques. Strikingly, we show that CML stem cells accumulate significantly higher levels of certain dipeptide species than normal HSCs. Once internalized, these dipeptide species activate amino-acid signalling via a pathway involving p38MAPK and the stemness transcription factor Smad3, which promotes CML stem cell maintenance. Importantly, pharmacological inhibition of dipeptide uptake inhibits CML stem cell activity in vivo. Our results demonstrate that dipeptide species support CML stem cell maintenance by activating p38MAPK–Smad3 signalling in vivo, and thus point towards a potential therapeutic target for CML treatment.

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confidence: 99%

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confidence: 99%

Dipeptide species regulate p38MAPK–Smad3 signalling to maintain chronic myelogenous leukaemia stem cells

et al. 2015

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PEPT (SLC15A) Family

Cited by 1 publication

References 84 publications

Dipeptide species regulate p38MAPK–Smad3 signalling to maintain chronic myelogenous leukaemia stem cells

Dipeptide species regulate p38MAPK–Smad3 signalling to maintain chronic myelogenous leukaemia stem cells

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