|
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 HMGA1(NM_001319078.2) 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.
Summary
This gene encodes a non-histone protein involved in many cellular processes, including regulation of inducible gene transcription, integration of retroviruses into chromosomes, and the metastatic progression of cancer cells. The encoded protein preferentially binds to the minor groove of A+T-rich regions in double-stranded DNA. It has little secondary structure in solution but assumes distinct conformations when bound to substrates such as DNA or other proteins. The encoded protein is frequently acetylated and is found in the nucleus. At least seven transcript variants encoding two different isoforms have been found for this gene.
Gene References into function
- HMG-I/Y is an oncogene important in the pathogenesis of human breast cancer
- during apoptosis of different types of tumor cells there is a monomethylation of the nuclear protein HMGA1a
- HMGI-Y physically interacts with Sp1 and C/EBP beta and facilitates the binding of both factors to the insulin receptor promoter
- HMGA1a is methylated in leukemia cells induced to undergo apoptosis
- HMGA1a expression was induced by hypoxia and accumulated in nuclear speckles with the endogenous splicing factor SC35. Overexpression of HMGA1a generated Presenilin-2V.
- expression and localization of HMGI(Y) in the subpopulations of placental tissue
- HMGA1 cooperates with either the N- or the C-terminal transcriptional activation domain of the estrogen receptor to stimulate estrogen response element binding and promoter transcriptional activity
- regulated dynamic properties of HMGA1a fusion proteins indicate that HMGA1 proteins are mechanistically involved in local and global changes in chromatin structure
- HMG-I(Y) expression may have a role in intrahepatic metastasis of hepatocellular carcinoma
- Examination of HMGA1a posttranslational modification patterns in breast cancer cell lines supports the existence of a dynamic biochemical switching mechanism for HMGA1a expressed in different ways in normal and malignant cells.
- HMGA1 positively regulates the human KL promoter in breast and ovarian cancer cells
- HMGA1 expression might have a role in human breast cancer
- study focuses on whether HMGA1a and HMGA1b proteins isolated from the same cell type have identical or different post-translational modifications patterns and whether these isoform patterns differ between non-malignant and malignant cells
- These results suggest hypoxia-induced signals in SK-N-SH cells lead to expression of HMGA1a, which may induce expression of the transcription factor N-Myc.
- sites of phosphorylation and the nature of methylation of HMGA1
- HMGA1 is translocated from the nucleus into the cytoplasm and mitochondria and associates with the regulatory D-loop region of the mitochondrial genome.
- HMGA1 as one of the first mediators in the development of human atherosclerotic plaques
- HMGA1 directly influences both the formation and repair of UV-induced DNA lesions in intact cells
- HMGA1 repression by RNA interference reduced neuroblastoma cell proliferation, indicating that HMGA1 is a novel MYCN target gene relevant for neuroblastoma tumorigenesis.
- NF-Y and HMG-I(Y) may play an important role in regulating the IL-10 promoter activity in B cells.
- mtDNA levels were reduced approximately 2-fold in HMGA1a over-expressing transgenic MCF-7 cells
- HMGA1 may be a novel molecular determinant of invasiveness and metastasis, as well as a potential therapeutic target, in pancreatic adenocarcinoma.
- Cytoplasmic relocalization of HIPK2 induced by HMGA1 overexpression is a mechanism of inactivation of p53 apoptotic function.
- Since HMGA1 regulates IR promoter activity, expression of IR gene was impaired causing reduction of IR on cell surface and that compromises with insulin sensitivity.
- Our results suggest that PRMT1 might be involved in the previously reported methylation of Arg25 in HMGA1a in vivo.
- HMGA1 proteins are involved in inhibiting XPA expression, resulting in increased UV sensitivity in cells that overexpress these proteins
- Fluorescence in situ hybridization was used to identify rearrangements of HMGA2 and its homologue HMGA1. HMGA1 rearrangement was not found in any of the cases
- HMGA1 nonhistone chromatin proteins, the SWI/SNF chromatin remodeling complexes, and sequence-specific transcription factors act together to regulate the expression of the CRYAB gene.
- HMGA1 disturbs retobblastoma protein (RB)-mediated cell arrest, suggesting a negative control of RB by HMGA1.
- HMGA1a is a sequence-specific RNA-binding factor causing sporadic Alzheimer's disease-linked exon skipping of presenilin-2 pre-mRNA
- the different profiles of HMGA1 protein expression in post-pubertal testicular tumours could represent a valuable diagnostic tool in some cases in which the histological differential diagnosis is problematic
- HMGA proteins are overexpressed in different tumors and the HMGA genes are often involved in chromosomal rearrangements [review]
- A previously unknown role for HMGA1 in the regulation of hNOS2, is demonstrated.
- HMGA1 overexpression is associated with pancreatic adenocarcinoma and promoted chemoresistance to gemcitabine
- HMGA1 promotes tumorigenicity through a PI3-K/Akt-dependent mechanism
- HMGA1 expression is necessary for the full expression of HPV18 E6 and E7 oncoproteins thus establishing a positive autoregulatory loop between HPV E6/E7 and HMGA1 expression.
- In primary human leukemia samples, there was a positive correlation between HMGA1a and STAT3 mRNA. Moreover, blocking STAT3 function in human leukemia or lymphoma cells led to decreased cellular motility and foci formation.
- an increased CCNB2 expression in human pituitary adenomas of different histotypes that is directly correlated with HMGA1 and HMGA2 expression.
