Disease relevance of INHBA

• Specific erythroid differentiation of mouse erythroleukemia cells by activins and its enhancement by retinoic acids [1].
• Inclusion criteria were SLV associated with thrombosis of the retinal artery; decrease in retinal blood flow (PSF: peak-systolic flow; EDF: end-diastolic flow velocity) and asymmetry between the two retinal arteries (>40%) documented by duplex scanning [2].
• Here we show that the overexpressed thyroid hormone receptor c-erbA effectively modulates erythroid differentiation and erythrocyte-specific gene expression in a T3-dependent fashion, when introduced into erythroid cells via a retrovirus [3].
• In addition, overexpression of PTP1B or treatment with CGP57148, a small molecule inhibitor of p210 bcr-abl, induced erythroid differentiation of K562 cells, a CML cell line derived from a patient in blast crisis [4].
• Modulation of retinoblastoma gene in normal adult hematopoiesis: peak expression and functional role in advanced erythroid differentiation [5].

Psychiatry related information on INHBA

• These novel observations indicate a coordinate expression and function of an inhibitory Id protein (Id2) and a stimulatory bHLH/bHLH heterodimer (TAL1/E2A) in normal erythroid differentiation [6].

High impact information on INHBA

• The beta-globin nuclear compartment in development and erythroid differentiation [7].
• mRNA silencing in erythroid differentiation: hnRNP K and hnRNP E1 regulate 15-lipoxygenase translation from the 3' end [8].
• In contrast, the endogenous thyroid hormone receptor does not detectably affect erythroid differentiation [3].
• The v-erbA oncogene, one of the two oncogenes of the avian erythroblastosis virus, efficiently blocks erythroid differentiation and suppresses erythrocyte-specific gene transcription [3].
• We conclude that progenitor cells committed to erythroid differentiation are present during the anemia of prematurity, and that the intrinsic responsiveness of the circulating BFU-E pool to erythropoietin is normal [9].

Chemical compound and disease context of INHBA

• Induction of erythroid differentiation in ouabain-resistant murine erythroleukemia cells by ouabain is reported [10].
• The effectiveness of purines and purine analogues as inducers of erythroid differentiation in cultured murine erythroleukemia cells has been investigated [11].
• Sodium butyrate and hemin induced erythroid differentiation in these leukemia cells as has already been shown with other erythroleukemia cells [12].
• Noncytotoxic concentrations of herbimycin A induced erythroid differentiation of K562 cells but not of murine erythroleukemia 745A cells [13].
• Changes in DNA associated with induction of erythroid differentiation by dimethyl sulfoxide in murine erythroleukemia cells [14].

Biological context of INHBA

• The porcine inhibin-alpha, -betaA (INHBA) and -betaB (INHBB) subunit genes have previously been mapped to chromosomes 15, 18 and 12, respectively [15].
• Dinucleotide repeat polymorphism in the INHBA gene [16].
• Using in vitro erythroid differentiation of CD34(+) primary cells, we obtained the main stages of early erythropoiesis, characterized at the molecular, biochemical, and functional levels [17].
• Apoptosis and erythroid differentiation can be induced in KU812 and K562 cells, respectively [18].
• Erythroid differentiation can be readily induced by butyric acid in cultured erythroleukemic cells in the presence of inhibitors of DNA synthesis and in the absence of cell division [19].

Anatomical context of INHBA

• Induction of differentiation of the human promyelocytic cell line HL-60 by activin/EDF [20].
• A human promyelocytic cell line, HL-60, treated with activin/EDF was found to differentiate into monocyte/macrophage-like cells [20].
• Thus, activin/EDF exerts its effect on hematopoietic cells not only on erythroid differentiation but also on at least a part of myeloid cell differentiation [20].
• Presence of activin (erythroid differentiation factor) in unfertilized eggs and blastulae of Xenopus laevis [21].
• The extracts from rat submandibular glands (SMGs) induced erythroid differentiation of K-562 [22].

Associations of INHBA with chemical compounds

• Butyric acid, a potent inducer of erythroid differentiation in cultured erythroleukemic cells [23].
• The observation that the binding of ouabain to the Na/K ATPase induces hemoglobin synthesis suggests that changes in the intracellular concentration of K+ ions may be involved in the control of erythroid differentiation in Friend erythroleukemic cells [10].
• Induction of erythroid differentiation in vitro by purines and purine analogues [11].
• DMSO, as well as a variety of other organic compounds, induce erythroid differentiation in Friend leukaemia (FL) cells [24].
• They accumulate embryonic and fetal haemoglobins on induction of erythroid differentiation with haemin, sodium butyrate or hydroxyurea [25].

Physical interactions of INHBA

• Stem cell factor influences the proliferation and erythroid differentiation of the MB-02 human erythroleukemia cell line by binding to a high-affinity c-kit receptor [26].
• Acquisition of heat shock factor 2 (HSF2) DNA binding activity is accompanied by induced transcription of heat shock genes in hemin-treated K562 cells undergoing erythroid differentiation [27].
• Erythroid differentiation of murine erythroleukemia (MEL) cells is far more extensive when the cells are attached to fibronectin-coated dishes than in suspension culture [28].
• These findings suggested that OCTN1 transports compound(s) that are required for erythroid differentiation, maturation, and/or growth [29].

Enzymatic interactions of INHBA

• However, RAP30 may have a role in regulating some alterations of transcription that accompany cellular differentiation; RAP30 is partially dephosphorylated when murine erythroleukemia cells are induced with dimethyl sulfoxide to undergo terminal erythroid differentiation [30].

Regulatory relationships of INHBA

• These results indicate that both p27KIP1 induction and regulation of GATA-1 play essential roles in activin A-induced erythroid differentiation and apoptosis [18].
• These results reveal a novel mechanism by which TAL1 activity is regulated and implicate acetylation of this transcription factor in promotion of erythroid differentiation [31].
• Furthermore, aberrant HOXA10 expression almost completely blocked erythroid differentiation in methylcellulose (P < .02) [32].
• SATB1 family protein expressed during early erythroid differentiation modifies globin gene expression [33].
• Transduction of a dominant-negative (dn) mutant of FADD inhibited caspase-8 activity and cell death and rescued BFU-E growth without abrogating erythroid differentiation [34].

Other interactions of INHBA

• Secretion of both VEGF-A and PlGF increases during in vitro erythroid differentiation [35].
• EDF is a homodimer with a Mr of 25,000; the Mr of the monomer is 15,500. cDNA clones encoding the Mr 15,500 subunit of EDF from THP-1 libraries were isolated and sequenced [36].
• Ectopic expression of a conditional GATA-2/estrogen receptor chimera arrests erythroid differentiation in a hormone-dependent manner [37].
• Constitutive activation of STAT5A promotes human hematopoietic stem cell self-renewal and erythroid differentiation [38].
• The SCL gene product: a positive regulator of erythroid differentiation [39].

Analytical, diagnostic and therapeutic context of INHBA

• Western analysis with an anti-beta A antibody and an erythroid differentiation bioassay confirmed that the conditioned media of LPS-activated monocytes contained the activin A/EDF protein [40].
• By using multiparameter flow cytometry, we have studied the ability of CD34+ cells expressing mutant N-RAS to undergo erythroid differentiation induced by erythropoietin [41].
• This globin expression pattern was not altered by the presence or absence of fetal bovine serum, vascular endothelial growth factor, Flt3-L, or coculture with OP-9 during erythroid differentiation and was not culture time dependent [42].
• Northern blotting analysis revealed that TIE was expressed preferentially in undifferentiated cell lines, especially when megakaryocytic, but not erythroid differentiation was induced [43].
• By Northern blot and Western blot analyses of murine splenic erythroblasts infected with the anemia-inducing strain Friend virus (FAV cells), RPS19 mRNA and protein expression were shown to decrease during terminal erythroid differentiation [44].

References