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The protein encoded by RLIM is a RING-H2 zinc finger protein. Additionally we are shipping RLIM Antibodies (61) and many more products for this protein.
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missense mutation in RLIM gene was identified in four males with intellectual disability from a three-generation family.
RNF12 is a novel positive regulator of p53 (show TP53 Proteins) pathway and an external E3 ubiquitin ligase (show MUL1 Proteins) for MDM2 (show MDM2 Proteins) destruction.
Rlim is a novel regulator of Stathmin (show STMN1 Proteins) protein in a ubiquitin-dependent manner, and represents a new pathway for malignant phenotype turnover by modulating the level of Stathmin (show STMN1 Proteins) protein in human osteosarcomas.
hus (show CFH Proteins) regulated nucleocytoplasmic shuttling of RLIM/Rnf12 coordinates cellular compartments during mammary alveolar cell survival
TP53 (show TP53 Proteins) does not directly bind to the RLIM promoter, it physically interacts with and prevents the binding of Sp1 (show PSG1 Proteins) to the RLIM promoter.
these results indicated that RLIM is an important positive regulator in TGF-beta (show TGFB1 Proteins) signaling pathway and cell migration.
RLIM represents a new pathway for telomere maintenance by modulating the level of TRF1 (show TERF1 Proteins) at telomeres.
These findings provide evidence for a dose-dependent role of RNF12 in the XCI counting and initiation process.
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.
In late preimplantation, Oct4 (show POU5F1 Proteins) 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.
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
results provide evidence that RLIM is dispensable for rXCI, indicating that in mice an RLIM-independent mechanism activates Xist in the embryo proper
The trans-activator RNF12 and cis (show CISH Proteins)-acting elements effectuate X chromosome inactivation independent of X-pairing.
RNF12 causes REX1 breakdown through dose-dependent catalysis, thereby representing an important pathway to initiate X-chromosome inactivation
Results provide strong evidence that RLIM/Rnf12 is required for the survival of differentiated milk-producing alveolar cells in pregnant and lactating female mice.
The X-inactivation trans-activator Rnf12 is negatively regulated by pluripotency factors in embryonic stem cells.
RNF12 is essential for initiation of XCI and is mainly involved in the regulation of Xist.
results assign crucial functions to the maternal deposit of Rnf12/RLIM for the initiation of imprinted X-chromosome inactivation
The protein encoded by this gene is a RING-H2 zinc finger protein. It has been shown to be an E3 ubiquitin protein ligase that targets LIM domain binding 1 (LDB1/CLIM), and causes proteasome-dependent degradation of LDB1. This protein and LDB1 are co-repressors of LHX1/LIM-1, a homeodomain transcription factor. Multiple alternatively spliced variants, encoding the same protein, have been identified.
E3 ubiquitin-protein ligase RLIM
, E3 ubiquitin-protein ligase RNF12
, LIM domain-interacting RING finger protein
, RING finger LIM domain-binding protein
, renal carcinoma antigen NY-REN-43
, ring finger protein 12
, ring zinc finger LIM domain binding protein
, ring zinc finger protein NY-REN-43antigen
, LIM domain interacting RING finger protein
, Hoxa1 regulated