Inhibitor of DNA Binding 4, Dominant Negative Helix-Loop-Helix Protein (ID4) Kits ELISA

Mouse (Murine) Inhibitor of DNA Binding 4, Dominant Negative Helix-Loop-Helix Protein (ID4) interaction partners

1. ID4 has a role in stem cell or progenitor capacity in spermatogonia and dictates the interface of transition between the different functional states

2. results indicate that Id4 marks spermatogonial stem cells in the mouse testis.

3. ID4 marks a stem cell-enriched subset of the mammary basal cell population. ID4 maintains the mammary stem cell pool by suppressing key factors required for luminal differentiation.

4. Id4 regulates NKX3.1, Sox9 and PTEN.

5. Id4 is a novel regulator of estrogen signaling, where Id4 restrains ERalpha (Montrer ESR1 Kits ELISA) expression in the basal and luminal cellular compartments of the mammary gland and regulates estrogen biosynthesis in the ovary

6. High expression levels of Id1 (Montrer ID1 Kits ELISA)-4 proteins may play important roles in regulating retinal progenitor cell proliferation and differentiation.

7. CpG-rich islands within the Id2 and Id4 genes were bound by PRMT5 and were hypomethylated in PRMT5-deficient cells, suggesting that PRMT5 plays a role in gene silencing during glial cell

8. ID4 promotes mammary gland development by suppressing p38MAPK (Montrer MAPK14 Kits ELISA) activity.

9. Study confirms the importance of the silencing of ID4 in murine and human CLL pathogenesis.

10. Id4 was identified as a key transcription factors enriched in the early phase of differentiation and affecting the differentiation of both osteoblasts and adipocyte cell types.

Zebrafish Inhibitor of DNA Binding 4, Dominant Negative Helix-Loop-Helix Protein (ID4) interaction partners

1. id4 appears to control the number of endocardial cells that contribute to the AV valves by regulating Wnt (Montrer WNT2 Kits ELISA) signaling in the developing AVC endocardium

Human Inhibitor of DNA Binding 4, Dominant Negative Helix-Loop-Helix Protein (ID4) interaction partners

1. These findings indicate that ID4 acts as a tumour suppressor in myeloid malignancies, and ID4 methylation is a potential biomarker in predicting disease progression and treatment outcome.

2. results highlight a key role for MALAT1 in control of VEGFA (Montrer VEGFA Kits ELISA) isoforms expression in breast cancer cells expressing gain-of-function mutant p53 (Montrer TP53 Kits ELISA) and ID4 proteins.

3. Study demonstrates that ID4, can promote p53 (Montrer TP53 Kits ELISA)- dependent apoptosis and senescence in prostate cancer cells by specifically modifying the acetylation of p53 (Montrer TP53 Kits ELISA), which increases its transcriptional activity and promotes the expression of pro-apoptotic and cell cycle regulatory genes.

4. The cellular uptake of inhibitor of DNA binding 4 protein (ID4) resulted in increased apoptosis, decreased proliferation and colony formation.

5. Several lines of evidence suggest ID4 may suppress BRCA1 function in basal-like breast cancer (BLBC) and in doing so, define a subset of BLBC patients who may respond to therapies traditionally used in BRCA1-mutant cancers. This review highlights recent advances in our understanding of the requirement for ID4 in mammary lineage commitment and the role for ID4 in BLBC.

6. The expression of Id4 protein was up-regulated in tumor tissues from hepatocellular carcinoma (HCC) patients, and overexpression of Id4 promoted HCC cell proliferation, clonogenicity in vitro, and tumorigenicity in vivo.

7. ID4 selectively regulates AR activity through direct interaction with FKBP52 (Montrer FKBP4 Kits ELISA).

8. High ID4 expression is associated with basal breast cancer.

9. A cell-autonomous positive-signaling circuit is associated with the PDGFB (Montrer PDGFB Kits ELISA)-NO-ID4-regulatory axis in glioblastoma cells.

10. ID4 expression induces AR expression in PC3 (Montrer PCSK1 Kits ELISA) cells, which generally lack AR. ID4 expression increased apoptosis and decreased cell proliferation and invasion.