Disease relevance of PROM1

• In the present study, molecular genetic analyses of a pedigree segregating for autosomal recessive retinal degeneration indicated that the affected individuals were homozygous for a nucleotide 1878 deletion in PROML1 [1].
• Expression of AC133, a novel hematopoietic precursor antigen, on acute myeloid leukemia cells [2].
• Prominin-1/CD133, a neural and hematopoietic stem cell marker, is expressed in adult human differentiated cells and certain types of kidney cancer [3].
• The purified CD133(+) cells highly engrafted NOD/SCID mice [4].
• Furthermore, in 4 proliferating hemangiomas, we showed that 0.14% to 1.6% of CD45(-) nucleated cells were EPCs that coexpressed CD133 and the EC marker KDR [5].
• These findings constitute the first conclusive evidence that CD133 stem cell antigen expression correlates with patient survival in gliomas, lending support to the current cancer stem cell hypothesis [6].

Psychiatry related information on PROM1

• CONCLUSIONS: Although retaining the cerclage prolonged the latency period between PROM and delivery, that benefit was more than offset by a greatly increased perinatal mortality rate [7].
• A matched case-control study was undertaken to determine whether dietary habits, prepregnancy weight, and weight gain during pregnancy were associated with increased risks for PROM [8].

High impact information on PROM1

• Subtracting the Math: prominin-positive cerebellar stem cells in white matter [9].
• Here we report that a subpopulation of circulating cells expressing AC133, a well-characterized marker of hematopoietic stem cells, also expresses early myogenic markers [10].
• Freshly isolated, circulating AC133(+) cells were induced to undergo myogenesis when cocultured with myogenic cells or exposed to Wnt-producing cells in vitro and when delivered in vivo through the arterial circulation or directly into the muscles of transgenic scid/mdx mice (which allow survival of human cells) [10].
• Human circulating AC133(+) stem cells restore dystrophin expression and ameliorate function in dystrophic skeletal muscle [10].
• Here, we further dissected the ALDH(hi)-Lin- population by selection for CD133, a surface molecule expressed on progenitors from hematopoietic, endothelial, and neural lineages [11].

Chemical compound and disease context of PROM1

• CONCLUSION: Patients receiving pentoxifylline demonstrated improved AROM, PROM, and muscle strength and decreased limb edema and pain [12].
• At the molecular level, prominin specifically interacts with membrane cholesterol and is a marker of a novel type of cholesterol-based lipid 'raft'. A frameshift mutation in the human prominin gene, which results in a truncated protein that is no longer transported to the cell surface, is associated with retinal degeneration [13].
• The first principle, which is accepted by most, consists of searching for a positive history of PROM, confirming PROM (by speculum examination, pooling, positive Nitrazine testing, and ferning), and obtaining cervical and vaginal cultures (for group B streptococcus/gonococcus and chlamydia) [14].
• For the purpose of evaluating fetal morbidity and mortality, group 1 included women with hypertensive disorders of pregnancy (preeclampsia or chronic hypertension), PROM, cocaine abuse, and > 20% abruptio placentae without regard to fetal status on admission (reassuring, nonreassuring, or stillborn) [15].
• None of the clinical prognostic markers such as age, hemogram, lactate dehydrogenase, and chromosomal aberration were significantly different between AC133(+) and AC133(-) leukemias [16].

Biological context of PROM1

• Here, we demonstrate, by using a novel prominin-1 antiserum (alphahE2), that the decrease of AC133 immunoreactivity observed during differentiation of the colonic adenocarcinoma-derived Caco-2 cells is not paralleled by a down-regulation of prominin-1 [3].
• These observations suggest that only the AC133 epitope is down-regulated upon cell differentiation [3].
• Under defined serum-free conditions, the growth factors requirements, proliferation, and differentiation capacity of muscle and neural hematopoiesis were distinct to that derived from committed hematopoietic sites and were uniquely restricted to CD45(-)CD34(-) cells expressing the prominin AC133 [17].
• The primary outcome measurement was change in physical impairments thought to be secondary to radiation, including active and passive range of motion (AROM and PROM), muscle strength, limb edema, and pain [12].
• Moreover, valproic acid treatment increases histone H4 acetylation levels at specific regulatory sites on HOXB4, a transcription factor gene with a key role in the regulation of HSC self-renewal and AC133, a recognized marker gene for stem cell populations [18].

Anatomical context of PROM1

• The CD34(dim) and AC133(-) population has been shown to contain the remaining progenitor cells [19].
• AC133-selected cells engraft successfully in a fetal sheep transplantation model, and human cells harvested from chimeric fetal sheep bone marrow have been shown to successfully engraft secondary recipients, providing evidence for the long-term repopulating potential of AC133(+) cells [19].
• Immunocytochemistry revealed that prom is concentrated in the plasma membrane evaginations at the base of the outer segments of rod photoreceptors [1].
• AC133 is one of a new panel of murine hybridoma lines producing monoclonal IgG antibodies (mAbs) to a novel stem cell glycoprotein antigen with a molecular weight of 120 kD [19].
• We have also shown that alphahE2 immunoreactivity, but not AC133 immunoreactivity, is present in several adult human tissues, such as kidney proximal tubules and the parietal layer of Bowman's capsule of juxtamedullary nephrons, and in lactiferous ducts of the mammary gland [3].

Associations of PROM1 with chemical compounds

• Selection based on CD133 and high aldehyde dehydrogenase activity isolates long-term reconstituting human hematopoietic stem cells [11].
• Here, we have cloned ABCB5, a rhodamine efflux transporter and novel member of the human P-glycoprotein family, which marks CD133-expressing progenitor cells among human epidermal melanocytes and determines as a regulator of membrane potential the propensity of this subpopulation to undergo cell fusion [20].
• Identification and characterization of a novel testosterone-regulated prominin-like gene in the rat ventral prostate [21].
• Hemodialysis is quantified as the Kt/V, calculated prom pre- and post-dialysis urea samples [22].
• Prominin: a story of cholesterol, plasma membrane protrusions and human pathology [13].

Regulatory relationships of PROM1

• AC133 antigen is selectively expressed on CD34(bright) hematopoietic stem and progenitor cells (progenitors) derived from human fetal liver and bone marrow, and blood [19].
• TGFBR3 knockdown led to focus formation and enhanced expression of CD133, a marker found on prostate cancer stem cells [23].
• In addition, ocular VHL lesions expressed several stem cell markers including CD133 to various degrees [24].
• Approximately, 60 +/- 8% of CD133 expressing cells expressed nestin [25].

Other interactions of PROM1

• These adherent cells did not express CD34 or CD133 antigens on their surface, nor did they express markers for endothelial, mesenchymal, or dendritic cells [4].
• Subsequent isolation and plating of nonadherent FL-derived VEGFR-2(+) cells with VEGF and FGF-2 resulted in differentiation of AC133(+ )VEGFR-2(+) cells into adherent AC133(-)VEGFR-2(+)Ac-LDL(+ )(acetylated low-density lipoprotein) colonies (plating efficiency of 3%) [26].
• EPCs labeled with CD34, CD133, and vascular endothelial growth factor receptor-2 (VEGFR2) antibodies were counted by flow cytometry in the peripheral blood of 53 NSCLC patients [27].
• CD45 and CD14 decreased, while CD34 and the progenitor-cell marker CD133 remained strongly expressed [28].
• Suppression of the growth of AC133/CD133 positive stem cells might be considered as one of the therapeutic targets for VHL-associated hemangioblastoma [24].

Analytical, diagnostic and therapeutic context of PROM1

• AC133 antibody provides an alternative to CD34 for the selection and characterization of cells necessary for both short- and long-term engraftment, in transplant situations, for studies of ex vivo expansion strategies, and for gene therapy [19].
• Progenitor cells coexpressing CD133 and CD34 were detected by flow cytometry in 11 of 12 proliferating hemangioma specimens from children 3 to 24 months of age [5].
• By both immunofluorescence and immunoprecipitation, the AC133 antigen was found to be expressed on the surface of Caco-2 cells [29].
• Human EPCs were isolated from donated buffy coats by magnetic microbeads and flow cytometry cell sorting using CD133 and VEGFR-2, respectively, as markers [30].
• Co-expression in CD34+ve cells markers of differentiation (Thy1, CD133, CXCR4, c1qRp) were investigated on CD34+ve cells by double direct immunofluorescence [31].

References