The proximal cis‐regulatory region of the RHD/RHCE promoter is 105 bp and contains a 55‐bp core devoid of known binding motifs but necessary for transcription

  title={The proximal cis‐regulatory region of the RHD/RHCE promoter is 105 bp and contains a 55‐bp core devoid of known binding motifs but necessary for transcription},
  author={Gregory Andrew Denomme and Duncheng Wang and Kimberly Matheson and Danny Titolo},
BACKGROUND: The RhD and RhCE polypeptides are erythroid‐specific members of the RH gene family. Little is known about the promoter cis‐regulatory proximal region responsible for transcription. 
2 Citations

Molecular basis for D− Japanese: identification of novel DEL and D− alleles

The occurrence of D− is approximately 0·5% in Japanese, but DEL in apparently D− individuals is relatively common compared with that in Caucasian populations. On the basis of molecular genetics, we



RHCE represents the ancestral RH position, while RHD is the duplicated gene.

In 2000, it was shown that the structure of the RH locus is an example for a gene cluster; RHD and RHCE face each other by their 3′ tail ends, and a third gene, SMP1 , was found to be interspersed between the 2 rhesus genes.

Erythroid‐specific activity of the glycophorin B promoter requires GATA‐1 mediated displacement of a repressor.

Using a cotransfection assay, it is found that hGATA‐1 can efficiently activate transcription of the −95 GPB construct in non‐erythroid cells and can remove repression of the GPB promoter by displacement of the ubiquitous proteins.

Aly/ REF, a factor for mRNA transport, activates RH gene promoter function

Aly/REF might be a novel transcription cofactor for erythroid‐specific genes and provide second proof of Aly/REF as a transcription coactivator, initially identified as a coactivators for the TCRα enhancer function.

Organization of the gene (RHCE) encoding the human blood group RhCcEe antigens and characterization of the promoter region.

Putative binding sites for SP1, GATA-1, and Ets proteins, nuclear factors known to be involved in the erythroid and megakaryocytic gene expression, were identified in this Rh promoter.

Interaction of Sp1 with the growth- and cell cycle-regulated transcription factor E2F

In vivo footprinting experiments indicated that both the sp1 and E2F binding sites are occupied throughout the cell cycle, in line with the hypothesis that E 2F functions as a growth- and cell cycle regulated tethering factor between Sp1 and the basic transcription machinery.

Cloning and characterization of erythroid-specific DNase I-hypersensitive site in human rhesus-associated glycoprotein gene.

The results suggest that the 5'-flanking sequence of RHAG gene is a preferable target sequence for retroviral transposition and that the enhancer was inserted in the same manner, resulting in the acquisition of erythroid dominant expression.

Erythroid regulatory elements

Erythroid differentiation leads to the production of red blood cells that contain a high level of hemoglobin, which is mainly regulated by glo‐bin gene transcription during development and differentiation, and combinations of three motifs, CCACC, SP1 and GATA represent the core elements of their regulatory sequences.

RHD gene deletion occurred in the Rhesus box.

The molecular structure of the RH gene locus explains the mechanisms for generating RHD/RHCE hybrid alleles and the RHD deletion.

T Cell-specific Expression of the MurineCD3δ Promoter*

The combination of NERF-2, Elf-1, and Ets-1 are expressed preferentially in lymphocytes and YY1 represses the promoter activity strongly in non-T cells, it is concluded that the combination of these transcription factors contributes to the T cell-specific expression pattern of mouseCD3δ.

Differential expression of the LYL, SCL and E2A helix-loop-helix genes within the hemopoietic system.

The low or undetectable expression of both SCL and LYL in most T lymphoid cell sources is consistent with the view that the translocations of these genes in human T cell leukemias alter their normal regulation and may thereby contribute to neoplasia.