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Validated All-in-One™ qPCR Primer for FOXP1(NM_001244814.3) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene belongs to subfamily P of the forkhead box (FOX) transcription factor family. Forkhead box transcription factors play important roles in the regulation of tissue- and cell type-specific gene transcription during both development and adulthood. Forkhead box P1 protein contains both DNA-binding- and protein-protein binding-domains. This gene may act as a tumor suppressor as it is lost in several tumor types and maps to a chromosomal region (3p14.1) reported to contain a tumor suppressor gene(s). Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq].
Gene References into function
- The FOXP1 winged helix transcription factor is a novel candidate tumor suppressor gene on chromosome 3p.
- Foxp1, although broadly expressed, is further regulated by tissue-specific alternative splicing of its functionally important sequence domains
- complex regulatory mechanism underlying Foxp1, Foxp2, and Foxp4 activity, demonstrating that Foxp1, Foxp2, and Foxp4 are the first Fox proteins reported whose activity is regulated by homo- and heterodimerization
- FOXP1 and FOXP2 expression patterns in human fetal brain are strikingly similar to those in the songbird, including localization to subcortical structures that function in sensorimotor integration and the control of skilled, coordinated movement
- FOXP1 is a potential ER coregulator in human breast carcinoma and may also independently regulate additional important pathways that control the progression of breast cancer
- Integrin engagement regulates monocyte differentiation through FOXP1.
- This study identifies FOXP1 as a new translocation partner of IGH in a site-dependent subset of MALT lymphomas.
- Results suggest that FOXP1 expression may be important in diffuse large B-cell lymphoma (DLBCL) pathogenesis.
- The heterogeneity of FOXP1 expression in germinal centre-derived lymphomas, may have more to do with the transforming events underlying these distinct types of lymphoma than with their common origin.
- Tumors with exclusively cytoplasmic expression of FOXP1 were linked with deep myometrial invasion.
- FOXP1 expression is an independent prognostic factor in MALT lymphomas. A subgroup of nongerminal center DLBCLs (Diffuse Large B-Cell Lymphomas, those marked by FOXP1 expression and trisomy 3 and 18) might represent a large-cell variant of MALT lymphomas
- rearrangement of FOXP1 is detected in a subset of large B-cell lymphomas with extranodal presentation
- these data implicate specific members of the FOX family of TFs (FOXC1, C2, P1, P4, and O1A) not previously suggested in heart failure pathogenesis.
- Our results suggest that MALT1-specific translocations and FOXP1 rearrangements are not commonly involved in pathogenesis.
- There may be a hormonal and hypoxia independent regulatory mechanism coordinating the expression of HIFs, the AR, and FOXP1 in prostate tumors.
- Expression of the forkhead transcription factor FOXP1 is associated with that of estrogen receptor-beta in primary invasive breast carcinomas.
- The expression of potentially oncogenic smaller FOXP1 isoforms may resolve the previously contradictory findings that FOXP1 represents a favorable prognostic marker in breast cancer and an adverse risk factor in B-cell lymphomas.
- FOXP1 protein is present in human endometrium with evidence of cycle stage-dependent changes in expression. FOXP1 expression was found in endometriotic lesions but not in endometrial adenocarcinoma
- Mechanisms other than translocation and copy number changes are responsible for FOXP1 overexpression in lymphoma.
- FOXP1 directly interacts with androgen receptor (AR) and negatively regulates AR signaling ligand-dependently.
- There was an association between FOXP1 and diffuse large B-cell lymphoma: significant relationship between BCL2 expression and FOXP1 genetic abnormalities.