|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for ACVR1C(NM_145259.2) Search again
By 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.
Validated result:
Summary
ACVR1C is a type I receptor for the TGFB (see MIM 190180) family of signaling molecules. Upon ligand binding, type I receptors phosphorylate cytoplasmic SMAD transcription factors, which then translocate to the nucleus and interact directly with DNA or in complex with other transcription factors (Bondestam et al., 2001 [PubMed 12063393]).[supplied by OMIM].
Gene References into function
- cDNA cloning, expression studies and chromosome mapping
- ALK7 and its isoforms are expressed in human placentae of different stages of pregnancy and that their expression is developmentally regulated
- ALK7 induces apoptosis through activation of the traditional TGF-beta pathway components
- the Nodal-ALK7 pathway inhibits cell proliferation by inducing G(1) cell cycle arrest
- AB and activin B and is responsible for activin-mediated secretion of insulin from pancreatic beta cell line, MIN6.
- ALK7-induced apoptosis is at least in part through two Smad-dependent pathways, Bax/Bcl-2 and Xiap.
- GDF3 regulates adipose-tissue homeostasis and energy balance under nutrient overload in part by signaling through the ALK7 receptor
- The antiproliferative effect of Nodal/ALK7 on ovarian cancer cells is in part mediated by cyclin G2.
- One of the direct target genes in the ALK7 signaling pathway is the insulin gene in pancreatic beta-cells, and that PDX-1 is directly involved in this pathway through interaction with Smad2 and Smad3.
