抗Mouse (Murine) RBM24 抗体:
抗Rat (Rattus) RBM24 抗体:
抗Human RBM24 抗体:
Seb4 is a target of MyoD during myogenesis and is required for myogenic gene expression.
Both Rbm24a and Rbm24b are also required for normal somite and craniofacial development.
Rbm24 involving in the regulation of cardiac gene expression, sarcomeric assembly, and cardiac contractility.
rbm24b is a key developmental cardiac genes with unequal roles in cardiovascular formation.
Rbm24 may function as a regulator of cardiac fibrosis.
the p53-Rbm24 loop is critical for the heart development and may be explored for mitigating congenital heart diseases and heart failure.
Rbm24 may potentially function as a novel key regulator for the development of the eye, nasal epithelium, and inner ear in vertebrates.
These results revealed that Stk38 kinase catalyzes the phosphorylation of Rbm24 during sarcomerogensis and this orchestrates accurate sarcomere alignment.
Study suggests that p63 is regulated by RBM24 via mRNA stability, which gives an insight into understanding how posttranscriptional regulatory mechanisms contribute to p63 expression.
RBM24 is sufficient to mediate muscle-specific exon inclusion.
Rbm24 plays a crucial role in myogenic differentiation at least in part through a myogenin-dependent post-transcriptional regulatory pathway.
The host factor RBM24 is involved in pregenomic RNA (pgRNA) packaging.
The RBM24 is a novel host factor involved in HCV replication and may function at the switch from translation to replication.
Data suggests that RBM24 binds to coding region of CHRM2 to regulate mRNA stability in cardiomyocytes; RBM24appears to drive changes in alternative splicing and in production of alternative transcript isoforms. (RBM24 = RNA binding motif protein-24; CHRM2 = cholinergic receptor muscarinic 2)
RBM24 interacted with the 5' TR of HBV pregenomic RNA to block 80S ribosome assembly on HBV pgRNA and thus inhibited core protein translation, whereas the interaction between RBM24 and the 3' TR enhanced the stability of HBV RNA.
embryonic stem cell switching into the differentiation state can be initiated by a tissue-specific splicing regulator, Rbm24.
Our results show that tissue-specific expression of RBM24 can explain the neuron-specific aberrant splicing of IKBKAP exon 20 in familial dysautonomia, and that ectopic expression of RBM24 in neuronal tissue could be a novel therapeutic target of the disease.
RBM24 acts at least in part through upregulating the expression of miR-25, which in turn targets MALAT1 for degradation.
Authors have identified a new function of microRNA-222 leading to alteration of myogenic differentiation at the level of alternative splicing, and provided evidence that this effect is mediated by Rbm24 protein.
Rbm24 is a novel player in the p53 pathway, which may be explored to restore proper cell cycle control in p53-deficient tumors via p21.
it was found that this protein Rbm24 regulates myogenic differentiation via the p21 signal pathway.
Plays a role in myogenic differentiation by regulating MYOG levels. Binds to the 3'-UTR of MYOG mRNA and regulates its stability (By similarity).
RNA-binding motif protein 24-A
, RNA-binding protein 24-A
, RRM domain-containing protein SEB-4
, RRM-containing protein SEB-4
, RNA-binding protein 24
, RNA-binding motif protein 24
, RNA-binding region (RNP1, RRM) containing 1
, RNA binding motif protein 24
, RNA binding protein
, RNA-binding protein SEB-4
, RNA-binding region (RNP1, RRM) containing 6
, RNA-binding region-containing protein 6