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. Author manuscript; available in PMC: 2011 Jan 22.
Published in final edited form as: Biochem Biophys Res Commun. 2009 Dec 31;391(4):1769–1774. doi: 10.1016/j.bbrc.2009.12.151

Figure 1. Fold change of significantly regulated HRD genes after 1 (A), 2 (B) and 4 (C) weeks exposure to CIH or CCH with respect to normoxic levels.

Figure 1

Negative values indicate down-regulation and zero value non-significant regulation. Note that no gene was similarly regulated by CIH and CCH. Genes: Adrbk1 = Adrenergic receptor kinase, beta 1, Ank2/3 = Ankyrin 2/3, Cdh13/16/2 = Cadherin 13/16/2, Csrp3 = Cysteine and glycine-rich protein 3, Ctnnal1 = Catenin (cadherin associated protein), alpha-like 1, Cxadr = Coxsackievirus and adenovirus receptor, Dmpk = Dystrophia myotonica-protein kinase, Hdac5 = Histone deacetylase 5, Id2 = Inhibitor of DNA binding 2, Itpr1 = Inositol 1,4,5-triphosphate receptor 1, Jup = Junction plakoglobin, Kcnh2 = Potassium voltage-gated channel, subfamily H (eag-related), member 2, Nfatc3 = Nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 3, Pcdhgc3 = Protocadherin gamma subfamily C, 3, Sema3a = Sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3A, Slc25a20 = Solute carrier family 25 (mitochondrial carnitine/acylcarnitine translocase), member 20, Slc8a1 = Solute carrier family 8 (sodium/calcium exchanger), member 1, Tjp1/2 = Tight junction protein 1/2, Vcl = Vinculin, Vezt = Vezatin, adherens junctions transmembrane protein.