anti-CXXC Finger Protein 5 (CXXC5) Anticorps

Mouse (Murine) CXXC Finger Protein 5 (CXXC5) interaction partners

1. Retroviral insertional mutagenesis identifies the del(5q) genes, CXXC5, TIFAB and ETF1, as well as the Wnt pathway, as potential targets in del(5q) myeloid neoplasms.

2. recruits DNA demethylase Tet2 to regulate TLR7/9-elicited interferon response in plasmacytoid dendritic cells

3. Data show that the peptide binding pocket of the Dishevelled 1 (Dvl1) PDZ domain is stabilized upon CXXC finger 5 protein (CXXC5) binding.

4. The finding of this study indicate that the regulation of myelin genes expression by CXXC5 is important for forming myelin structure involved with axonal electrical signal transfer in the corpus callosum.

5. The Dishevelled-binding protein CXXC5 negatively regulates cutaneous wound healing.

6. CXXC5 is a transcriptional activator for Flk-1, mediating BMP signaling for differentiation and migration of endothelial cell and vessel formation.

Human CXXC Finger Protein 5 (CXXC5) interaction partners

1. NUDT21 inhibits HCC proliferation, metastasis and tumorigenesis, at least in part, by suppressing PSMB2 and CXXC5.

2. KANK1 inhibits Malignant peripheral nerve sheath tumors cell growth though CXXC5 mediated apoptosis.

3. show here that CXXC5 is an E2-ERalpha responsive gene regulated by the interaction of E2-ERalpha with an ERE present at a region upstream of the initial translation codon of the gene

4. High CXXC5 expression seems to affect several steps in human leukemogenesis, including intracellular events as well as extracellular communication.

5. Findings suggest that overexpression of CXXC5 in C2C12 myoblasts facilitated myocyte differentiation, while RNAi interference of CXXC5 significantly inhibited the differentiation of C2C12 myoblasts.

6. Low CXXC5 expression is associated with acute myeloid leukemia.

7. targeting of CXXC5/RINF should be considered as a possible therapeutic strategy, especially in high-risk patients who show increased expression in AML cells compared with normal hematopoietic cells

8. Lack of promoter hypermethylation or somatic mutations are found in the potential tumor suppressor CXXC5 in myelodysplastic syndromes or acute myeloid leukemia with deletion 5q.

9. RINF overexpression represents an independent molecular marker for poor prognosis in breast tumors.

10. RINF expression correlates with retinoid-induced differentiation of leukemic cells and with cytokine-induced myelopoiesis of normal CD34(+) progenitors.

11. These findings suggest that CF5 plays a crucial role in ATM-p53 signaling in response to DNA damage.