SLC25A28 | bioCADDIE Data Discovery Index
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Displaying 11 of 11 results for "SLC25A28"
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  1. MFRN2_DANRE UniProt:Swiss-Prot

    ID: Q7T292

    Description: Mitoferrin-2 Helical; Name=1 Helical; Name=2 Helical; Name=3 Helical; Name=4

  2. MFRN1_RAT UniProt:Swiss-Prot

    ID: Q66H23

    Description: Mitoferrin-1 Helical; Name=1 Helical; Name=2 Helical; Name=3 Helical; Name=4 Helical; Name=5 ...

  3. MFN2B_XENLA UniProt:Swiss-Prot

    ID: Q68F18

    Description: Mitoferrin-2B Helical; Name=1 Helical; Name=2 Helical; Name=3 Solcar

  4. MFN2A_XENLA UniProt:Swiss-Prot

    ID: Q6GLJ0

    Description: Mitoferrin-2A Helical; Name=1 Helical; Name=2 Helical; Name=3 Solcar

  5. MFRN_DICDI UniProt:Swiss-Prot

    ID: Q55DY8

    Description: Mitoferrin Helical; Name=1 Helical; Name=2 Helical; Name=3 Helical; Name=4 Helical; Name=5 He...

  6. MFRN_CAEEL UniProt:Swiss-Prot

    ID: Q23125

    Description: Mitoferrin Helical; Name=1 Helical; Name=2 Helical; Name=3 Helical; Name=4 Helical; Name=5 He...

  7. MFRN1_BOVIN UniProt:Swiss-Prot

    ID: Q3ZBJ8

    Description: Mitoferrin-1 Helical; Name=1 Helical; Name=2 Helical; Name=3 Solcar

  8. MFRN1_DANRE UniProt:Swiss-Prot

    ID: Q287T7

    Description: Mitoferrin-1 Helical; Name=1 Helical; Name=2 Helical; Name=3 Helical; Name=4 Helical; Name=5 ...

  9. Comprehensive expression profiling across primary fetal liver terminal erythroid differentiation OmicsDI

    ID: E-GEOD-20391

    Date Released: 05-01-2014

    Description: the homeodomain-interacting protein kinases 1 and 2, Hipk1 and Hipk2, are essential but redundant in hematopoietic development—because Hipk1/Hipk2 double-deficient animals exhibit severe defects in hematopoiesis and vasculogenesis while the single knockouts do not. These serine-threonine kinases phosphorylate, and consequently modify the functions of, several important hematopoietic transcription factors and cofactors. Here we show that Hipk2 knockdown alone plays a significant role in terminal fetal liver erythroid differentiation. Hipk1 and Hipk2 are highly induced during primary mouse fetal liver erythropoiesis. Specific knockdown of Hipk2 inhibits terminal erythroid cell proliferation—explained in part by impaired cell cycle progression as well as increased apoptosis—and terminal enucleation as well as the accumulation of hemoglobin. Hipk2 knockdown also reduces the transcription of many genes involved in proliferation and apoptosis as well as important, erythroid-specific gen...

  10. Comprehensive expression profiling across primary fetal liver terminal erythroid differentiation ArrayExpress

    ID: E-GEOD-20391

    Description: the homeodomain-interacting protein kinases 1 and 2, Hipk1 and Hipk2, are essential but redundant in hematopoietic development—because Hipk1/Hipk2 double-deficient animals exhibit severe defects in hematopoiesis and vasculogenesis while the single knockouts do not. These serine-threonine kinases phosphorylate, and consequently modify the functions of, several important hematopoietic transcription factors and cofactors. Here we show that Hipk2 knockdown alone plays a significant role in terminal fetal liver erythroid differentiation. Hipk1 and Hipk2 are highly induced during primary mouse fetal liver erythropoiesis. Specific knockdown of Hipk2 inhibits terminal erythroid cell proliferation—explained in part by impaired cell cycle progression as well as increased apoptosis—and terminal enucleation as well as the accumulation of hemoglobin. Hipk2 knockdown also reduces the transcription of many genes involved in proliferation and apoptosis as well as important, erythroid-specific gen...

  11. Comprehensive expression profiling across primary fetal liver terminal erythroid differentiation BioProject

    ID: PRJNA125517

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: the homeodomain-interacting protein kinases 1 and 2, Hipk1 and Hipk2, are essential but redundant in hematopoietic development—because Hipk1/Hipk2 double-deficient animals exhibit severe defects in hematopoiesis and vasculogenesis while the single knockouts do not. These serine-threonine kinases phosphorylate, and consequently modify the functions of, several important hematopoietic transcription factors and cofactors. Here we show that Hipk2 knockdown alone plays a significant role in terminal fetal liver erythroid differentiation. Hipk1 and Hipk2 are highly induced during primary mouse fetal liver erythropoiesis. Specific knockdown of Hipk2 inhibits terminal erythroid cell proliferation—explained in part by impaired cell cycle progression as well as increased apoptosis—and terminal enucleation as well as the accumulation of hemoglobin. Hipk2 knockdown also reduces the transcription of many genes involved in proliferation and apoptosis as well as important, erythroid-specific genes involved in h...

Displaying 11 of 11 results for "SLC25A28"