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Homo sapiens


Sequence variation: Heterozygous for TP53 p.His179Tyr (c.535C>T) and p.Arg282Trp (c.843_844CC>TT) (PubMed=8504475). Omics: Deep antibody staining analysis. Omics: Deep proteome analysis. Omics: Deep RNAseq analysis. Omics: Metabolome analysis. Omics: Transcriptome analysis. Caution: Although HaCaT is distributed by a number of sources, the only official DKFZ-approved supplier is CLS. Discontinued: BCRJ; 0341; true. Discontinued: DSMZ; ACC-771; true. Discontinued: ICLC; HL14001; true. DT Created: 04-04-12; Last updated: 06-09-19; Version: 27

Proper Citation

DSMZ Cat# ACC-771, RRID:CVCL_0038


Spontaneously immortalized cell line DT Created: 04-04-12; Last updated: 06-09-19; Version: 27


DT Created: 04-04-12; Last updated: 06-09-19; Version: 27


HaCAT, HACAT, Hacat DT Created: 04-04-12, Last updated: 06-09-19, Version: 27



Cat Num


Cross References

BTO; BTO:0000552 EFO; EFO_0002056 CLDB; cl7229 AddexBio; T0020001/117 BCRJ; 0341 CCRID; 3111C0001CCC000373 CCRID; 3142C0001000001712 CCTCC; GDC0106 ChEMBL-Cells; CHEMBL3308509 ChEMBL-Targets; CHEMBL614392 CLS; 300493/p800_HaCaT Cosmic; 1530737 DSMZ; ACC-771 GEO; GSE57080 GEO; GSM913344 GEO; GSM913345 GEO; GSM960278 GEO; GSM960279 GEO; GSM960280 GEO; GSM960286 GEO; GSM960287 GEO; GSM960288 GEO; GSM960294 GEO; GSM960295 GEO; GSM960296 GEO; GSM1375594 GEO; GSM1375595 GEO; GSM1375596 GEO; GSM1375597 GEO; GSM1375598 GEO; GSM1375599 GEO; GSM1375600 GEO; GSM1375601 GEO; GSM1375602 GEO; GSM1375603 GEO; GSM1375604 GEO; GSM1375605 GEO; GSM1861816 GEO; GSM1861817 GEO; GSM1861820 GEO; GSM1861821 GEO; GSM2112559 GEO; GSM2112563 GEO; GSM2495796 GEO; GSM2495797 GEO; GSM2495798 IARC_TP53; 1820 ICLC; HL14001 IZSLER; BS CL 168 KCB; KCB 200442YJ Lonza; 56 MetaboLights; MTBLS127 PRIDE; PXD000496 PRIDE; PXD000670 PRIDE; PXD002460 PRIDE; PXD007789 TOKU-E; 3890 Wikidata; Q5636366 DT Created: 04-04-12; Last updated: 06-09-19; Version: 27


DT Created: 04-04-12; Last updated: 06-09-19; Version: 27

Originate from Same Individual

DT Created: 04-04-12; Last updated: 06-09-19; Version: 27

Novel role for the testis-enriched HSPA2 protein in regulating epidermal keratinocyte differentiation.

  • Gogler-Pigłowska A
  • J. Cell. Physiol.
  • 2017 Dec 12

Literature context:


HSPA2, a poorly characterized member of the HSPA (HSP70) chaperone family, is a testis-enriched protein involved in male germ cell differentiation. Previously, we revealed that HSPA2 is present in human stratified epithelia, including epidermis, however the contribution of this protein to epithelial biology remained unknown. Here, we show for the first time that HSPA2 is expressed in basal epidermal keratinocytes, albeit not in keratinocytes exhibiting features attributed to primitive undifferentiated progenitors, and participates in the keratinocyte differentiation process. We found that HSPA2 is dispensable for protection of HaCaT keratinocytes against heat shock-induced cytotoxicity. We also shown that lentiviral-mediated shRNA silencing of HSPA2 expression in HaCaT cells caused a set of phenotypic changes characteristic for keratinocytes committed to terminal differentiation such as reduced clonogenic potential, impaired adhesiveness and increased basal and confluency-induced expression of differentiation markers. Moreover, the fraction of undifferentiated cells that rapidly adhered to collagen IV was less numerous in HSPA2-deficient cells than in the control. In a 3D reconstructed human epidermis model, HSPA2 deficiency resulted in accelerated development of a filaggrin-positive layer. Collectively, our results clearly show a link between HSPA2 expression and maintenance of keratinocytes in an undifferentiated state in the basal layer of the epidermis. It seems that HSPA2 could retain keratinocytes from premature entry into the terminal differentiation process. Overall, HSPA2 appears to be necessary for controlling development of properly stratified epidermis and thus for maintenance of skin homeostasis.

Ccdc3: A New P63 Target Involved in Regulation Of Liver Lipid Metabolism.

  • Liao W
  • Sci Rep
  • 2017 Aug 21

Literature context:


TAp63, a member of the p53 family, has been shown to regulate energy metabolism. Here, we report coiled coil domain-containing 3 (CCDC3) as a new TAp63 target. TAp63, but not ΔNp63, p53 or p73, upregulates CCDC3 expression by directly binding to its enhancer region. The CCDC3 expression is markedly reduced in TAp63-null mouse embryonic fibroblasts and brown adipose tissues and by tumor necrosis factor alpha that reduces p63 transcriptional activity, but induced by metformin, an anti-diabetic drug that activates p63. Also, the expression of CCDC3 is positively correlated with TAp63 levels, but conversely with ΔNp63 levels, during adipocyte differentiation. Interestingly, CCDC3, as a secreted protein, targets liver cancer cells and increases long chain polyunsaturated fatty acids, but decreases ceramide in the cells. CCDC3 alleviates glucose intolerance, insulin resistance and steatosis formation in transgenic CCDC3 mice on high-fat diet (HFD) by reducing the expression of hepatic PPARγ and its target gene CIDEA as well as other genes involved in de novo lipogenesis. Similar results are reproduced by hepatic expression of ectopic CCDC3 in mice on HFD. Altogether, these results demonstrate that CCDC3 modulates liver lipid metabolism by inhibiting liver de novo lipogenesis as a downstream player of the p63 network.

Sensing Self and Foreign Circular RNAs by Intron Identity.

  • Chen YG
  • Mol. Cell
  • 2017 Jul 20

Literature context:


Circular RNAs (circRNAs) are single-stranded RNAs that are joined head to tail with largely unknown functions. Here we show that transfection of purified in vitro generated circRNA into mammalian cells led to potent induction of innate immunity genes and confers protection against viral infection. The nucleic acid sensor RIG-I is necessary to sense foreign circRNA, and RIG-I and foreign circRNA co-aggregate in cytoplasmic foci. CircRNA activation of innate immunity is independent of a 5' triphosphate, double-stranded RNA structure, or the primary sequence of the foreign circRNA. Instead, self-nonself discrimination depends on the intron that programs the circRNA. Use of a human intron to express a foreign circRNA sequence abrogates immune activation, and mature human circRNA is associated with diverse RNA binding proteins reflecting its endogenous splicing and biogenesis. These results reveal innate immune sensing of circRNA and highlight introns-the predominant output of mammalian transcription-as arbiters of self-nonself identity.