Recombinant Human Colony Stimulating Factor 1 Receptor

• Cat.No.: CSF1R-1666H

Specification

• Cat. No.: CSF1R-1666H
• Description: Macrophage colony-stimulating factor (M-CSF, also termed CSF-1) receptor is an integral membrane tyrosine kinase, expressed in monocytes (macrophages and their progenitors) and drives growth and development of this blood cell lineage. It also triggers growth and development of mononuclear phagocytes and placental trophoblasts. M-CSF receptor is present in osteoclasts both at mRNA and protein levels. When M-CSF ligand specifically binds to the M-CSF receptor on osteoclasts, it induces receptor dimerization, activation and autophosphorylation of cytoplasmic tyrosine residues M-CSF and its receptor present as candidate therapeutic targets in states of inflammatory bone erosion.
• Source: Mammalian cells
• Molecular Weight: The predicted molecular weight of Recombinant Human M-CSF R is 81 kDa. However, as a result of glycosylation, the actual molecular weight of the monomer as observed by migration on SDS Page is 150 kDa.
• State Of Matter: Lyophilized.
• Purity: >97% by SDS Page and analyzed by silver stain.
• Endotoxin: <1.0 EU/µg as determined by the LAL method.
• Storage: This lyophilized protein is stable for six to twelve months when stored desiccated at -20℃ to -70℃. After aseptic reconstitution, this protein may be stored at 2℃ to 8℃ for one month or at -20℃ to -70℃ in a manual defrost freezer. Avoid Repeated Freeze Thaw Cycles. See Product Insert for exact lot specific storage instructions.
• Tag: Non

Gene Information

• Gene Name: CSF1R colony stimulating factor 1 receptor [ Homo sapiens ]
• Synonyms: CSF1R; colony stimulating factor 1 receptor; CSFR; FIM2; C-FMS; CD115; CD115 antigen; FMS proto-oncogene; macrophage colony stimulating factor I receptor; McDonough feline sarcoma viral (v-fms) oncogene homolog; Macrophage colony-stimulating factor 1 receptor; CSF-1-R; EC 2.7.10.1; c-fms; soluble CSF1R variant 1
• Gene ID: 1436
• mRNA Refseq: NM_005211
• Protein Refseq: NP_005202
• MIM: 164770
• UniProt ID: P07333
• Chromosome Location: 5q32
• Pathway: Cytokine-cytokine receptor interaction; Endocytosis; Hematopoietic cell lineage; Pathways in cancer
• Function: ATP binding; cytokine binding; macrophage colony stimulating factor receptor activity; nucleotide binding; protein homodimerization activity; receptor activity; transferase activity

Reviews

01/09/2022

With its remarkable quality, reliability, and the manufacturer's excellent technical support, I am confident that it will be an invaluable asset in driving my scientific inquiries forward and facilitating groundbreaking discoveries in my field.

10/30/2017

This variety allows me to select the most appropriate option based on the specific requirements of my research.

03/10/2017

the manufacturer's commitment to quality control and rigorous testing guarantees the reliability and reproducibility of the CSF1R protein, which is essential for obtaining accurate and consistent results.

Q&As

Are there any FDA-approved drugs targeting CSF1R for clinical use?

Yes, drugs like pexidartinib have been approved for the treatment of certain rare tumors called tenosynovial giant cell tumors (TGCT) that overexpress CSF1R.

How can CSF1R inhibitors impact the tumor microenvironment?

CSF1R inhibitors can modulate the tumor microenvironment by reducing the number of tumor-associated macrophages and promoting an anti-tumor immune response.

Can CSF1R inhibitors be used in combination with other cancer treatments?

Yes, CSF1R inhibitors are often used in combination with chemotherapy and immunotherapy to enhance treatment effectiveness.

What are the potential clinical applications of CSF1R inhibitors?

CSF1R inhibitors are being investigated for cancer therapy to block tumor-promoting macrophages and slow down cancer progression.

Can CSF1R inhibitors be used to treat neurodegenerative diseases?

Research is ongoing, and CSF1R inhibitors are being explored as a potential therapy for neurodegenerative diseases, but no FDA-approved treatments currently exist.