IGF1R Antibodies

Insulin-like growth factor 1 receptor (IGF1R)

Receptor tyrosine kinase which mediates actions of insulin-like growth factor 1 (IGF1). Binds IGF1 with high affinity and IGF2 and insulin (INS) with a lower affinity.

The activated IGF1R is involved in cell growth and survival management. IGF1R is crucial for tumor survival and transformation of malignant cell.

Gene Information

Human
Gene Name:	IGF1R
Uniprot:	P08069
Entrez:	3480

Family

Belongs to:
protein kinase superfamily

Alternative Names

CD221 antigen; CD221; EC 2.7.10; EC 2.7.10.1; IGF1R; IGF-1R; IGF-I R; IGF-I receptor; IGFIR; IGF-IR; IGFR; insulin-like growth factor 1 receptor; Insulin-like growth factor I receptor; JTK13; MGC142170; MGC142172; MGC18216; soluble IGF1R variant 1; soluble IGF1R variant 2

Molecular Weight

Mass (kDA):
154.793 kDA

Genomic Context

Human
Location:	15q26.3
Sequence:	15; NC_000015.10 (98648539..98964530)

Tissue Specificity

Found as a hybrid receptor with INSR in muscle, heart, kidney, adipose tissue, skeletal muscle, hepatoma, fibroblasts, spleen and placenta (at protein level). Expressed in a variety of tissues. Overexpressed in tumors, including melanomas, cancers of the colon, pancreas prostate and kidney.

Subcellular Localizations

Cell membrane; Single-pass type I membrane protein.

Diseases

• Malignant Neoplasms
• Neoplasms
• Malignant Neoplasm Of Breast
• Mammary Neoplasms
• Neoplasm Metastasis
• Carcinoma
• Growth Retardation
• Malignant Paraganglionic Neoplasm
• Cell Transformation, Neoplastic
• Fetal Growth Retardation
• Dwarfism
• Diabetes Mellitus

• Insulin Resistance
• Growth Disorders
• Adenocarcinoma
• Hypertrophy
• Cell Invasion
• Lung Neoplasms

Interacting Proteins

• ARHGEF12
• CAMP
• Crk
• CSK
• CTNNB1

• IGF1
• KCNIP3
• LEF1
• MDM2
• PIK3R1

• PIK3R3
• PPM1A
• PTPN1
• PTPN11
• PTPN6

• TAGLN

Pathways

• Cell Proliferation
• Cell Growth
• Pathogenesis
• Aging
• Cell Cycle
• Cell Death
• Secretion
• Localization
• Gene Silencing
• Angiogenesis
• Cell Migration
• Rna Interference
• Methylation

• Translation
• Insulin Secretion
• Cell Differentiation
• Dna Methylation
• Endocytosis
• Glycolysis
• Transport

PTMs

• Phosphorylation
• Methylation
• Cleavage
• Demethylation

• Oxidation
• Ubiquitination
• Glycosylation
• Acetylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/IGF1R

Best Uses Of The IGF1R Marker In SCAPs

In this article, we'll discuss Boster Bio: hsa-let-7c and IGF1R expression in SCAPs. We will also talk about immunofluorescence and ICC. We will also look at Boster's validation procedure. ICC is the most commonly used method for IGF1R analysis. ICC is a reliable method to detect IGF1R-related expression in many cell types that include SCAPs.

BosterBio: hsa-let-7c

Let-7c, a microRNA thought to suppress tumor growth, has been found to have biological properties that can be utilized to treat cancer cells. It could also play a role in mesenchymal stem cell differentiation. Let-7c expression levels were analyzed in human dental pulp-derived mesenchymal stem cells (DPMSCs) treated with insulin-like growth factor I. However let-7c did not significantly alter the viability of cells.

DPMSCs with and without IGF1R expression had lower levels of Let-7c. Let-7c was expressed at lower levels in DPMSCs with -Let-7c than in +Let-7c DPMSCs. Let-7c expression decreased from day 3 to day 7 in both groups. Additionally, let-7c expression significantly reduced from day 3 to day 7.

Let-7c is a posttranscriptional controller of gene expression that targets the 3'-UTR regions of the mRNAs targeted. TargetScan predicted that let-7c binds to the IGF-1R mRNA. Let-7c blocked the osteo/odontogenic differentiation induced by IGF-1 in DPMSCs by reducing the IGF-1R mRNA expression on membranes. This inhibition was correlated with diminished MAPK signaling pathways of JNK/P38.

Expression of IGF1R in SCAPs.

We investigated the role of the IGF-1/IGF1R/hsa-let-7c axis in SCAPs differentiation and proliferation. We conducted western blots on cells' cytoplasmic proteins at 0.5, one, and six hours following transfection. We observed that ERK and JNK were nearly constant while the p38 protein was virtually impossible to detect. Our results suggested that SCAPs treated by IGF-1 were not distinguished.

Isolated SCAPs displayed spindle-like morphology. They were positive for STRO-1 which is a marker for mesenchymal stem cells. The CD73 and CD90 expressions were high, and the CD45 and CD74 expression was low. Nodule staining was also performed. The cells didn't express IGF1R this suggests that SCAPs were not infected by hematopoietic cell lines.

Interestingly, the IGF-1/IGF-1R/hsa-let-7c axis played a major role in regulating the odonto/osteogenic differentiation of SCAPs. The downstream signaling pathways of MAPK pathway were affected by the expression of IGF-1R. Further studies are needed to understand how the IGF-1/IGF1R/hsa-let-7c axis regulates SCAP differentiation.

Researchers discovered 92 GIST patients who had untreated advanced stage disease and low response rates in a study in 2012. They examined the expression of the p-IGF1R (Y1316) and MMP3, two signaling molecules involved in the immune system. Their study showed that the expression of pIGF1R was associated with a worse response rate and a lower progression-free survival.

While we are aware of the significance of insulin-like growth factors receptor type 1 in the treatment of cancer, the clinical outcomes for treatments that target this receptor are mixed. The classic model of the IGF1R's role in cancer has been based on an ON/OFF ligand-receptor interaction and ubiquitin's downregulation was believed to be an integral partnd-rreahration. Howeve,s recn't exdermdentalidaa igahvered in cancer cells and thirs receptois suggesd that the trdditionac modelhiscovellys imoliihed.

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