Ring Finger Protein, LIM Domain Interacting Proteine (RLIM)

Human Ring Finger Protein, LIM Domain Interacting (RLIM) Interaktionspartner

1. Results from a study on gene expression variability markers in early-stage human embryos shows that RLIM is a putative expression variability marker for the 3-day, 8-cell embryo stage.

2. missense mutation in RLIM gene was identified in four males with intellectual disability from a three-generation family.

3. RNF12 is a novel positive regulator of p53 (zeige TP53 Proteine) pathway and an external E3 ubiquitin ligase (zeige MUL1 Proteine) for MDM2 (zeige MDM2 Proteine) destruction.

4. Rlim is a novel regulator of Stathmin (zeige STMN1 Proteine) protein in a ubiquitin-dependent manner, and represents a new pathway for malignant phenotype turnover by modulating the level of Stathmin (zeige STMN1 Proteine) protein in human osteosarcomas.

5. hus (zeige CFH Proteine) regulated nucleocytoplasmic shuttling of RLIM/Rnf12 coordinates cellular compartments during mammary alveolar cell survival

6. TP53 (zeige TP53 Proteine) does not directly bind to the RLIM promoter, it physically interacts with and prevents the binding of Sp1 (zeige PSG1 Proteine) to the RLIM promoter.

7. these results indicated that RLIM is an important positive regulator in TGF-beta (zeige TGFB1 Proteine) signaling pathway and cell migration.

8. RLIM represents a new pathway for telomere maintenance by modulating the level of TRF1 (zeige TERF1 Proteine) at telomeres.

9. These findings provide evidence for a dose-dependent role of RNF12 in the XCI counting and initiation process.

Mouse (Murine) Ring Finger Protein, LIM Domain Interacting (RLIM) Interaktionspartner

1. These findings show that control of Lhx2 (zeige LHX2 Proteine) function by Ldb1 (zeige LDB1 Proteine) and Rnf12 underpins the coordinated differentiation of neurons and Muller glia in postnatal retina.

2. These results reveal crucial roles of Rlim for the maintenance of high Xist RNA levels, Xist clouds and X-silencing in female embryos at blastocyst stages, while initial Xist expression appears Rlim-independent.

3. In late preimplantation, Oct4 (zeige POU5F1 Proteine) served as a chromatin opener to create transcriptional permissive states at Xm-Xist/Tsix genomic loci. In parthenogenetic embryos, Rnf12 overdose caused Xm-Xist derepression via Xm-Tsix repression; physiological Rnf12 levels were essential for Xm-Xist silencing maintenance in fertilized embryos.

4. high RNF12 levels may contribute to the specific activation of maternal Xist in XpDeltaXist female ROSI embryos, but upregulation of additional Xp derived factors and/or the specific epigenetic constitution of the round spermatid-derived Xp are expected to be more critical

5. results provide evidence that RLIM is dispensable for rXCI, indicating that in mice an RLIM-independent mechanism activates Xist in the embryo proper

6. The trans-activator RNF12 and cis (zeige CISH Proteine)-acting elements effectuate X chromosome inactivation independent of X-pairing.

7. RNF12 causes REX1 breakdown through dose-dependent catalysis, thereby representing an important pathway to initiate X-chromosome inactivation

8. Results provide strong evidence that RLIM/Rnf12 is required for the survival of differentiated milk-producing alveolar cells in pregnant and lactating female mice.

9. The X-inactivation trans-activator Rnf12 is negatively regulated by pluripotency factors in embryonic stem cells.

10. RNF12 is essential for initiation of XCI and is mainly involved in the regulation of Xist.