gbp-1

Galectin-1 Protein, Human, Recombinant is expressed in E. coli expression system. The predicted molecular weight is 15 kDa and the accession number is A0A384MR27.

Galectin 1(Gal-1), a β-galactoside binding mammalian lectin of 14KDa, is implicated in many signalling pathways, immune responses associated with cancer progression and immune disorders. Inhibition of human Gal-1 has been regarded as one of the potential therapeutic approaches for the treatment of cancer, as it plays a major role in tumour development and metastasis by modulating various biological functions viz. apoptosis, angiogenesis, migration, cell immune escape.

Galectin-1 Protein, Human, Recombinant (His) is expressed in E. coli expression system with His tag. The predicted molecular weight is 16.07 kDa and the accession number is NP_002296.1.

Galectin 1 (Gal-1), a β-galactoside binding mammalian lectin of 14KDa, is implicated in many signalling pathways, immune responses associated with cancer progression and immune disorders. Inhibition of human Gal-1 has been regarded as one of the potential therapeutic approaches for the treatment of cancer, as it plays a major role in tumour development and metastasis by modulating various biological functions viz. apoptosis, angiogenesis, migration, cell immune escape.

Adiponectin Protein, Cynomolgus, Recombinant (His) is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 25.76 kDa and the accession number is A0A2K5X7X6.

Adiponectin Protein, Human, Recombinant (His) is expressed in Baculovirus insect cells with His tag. The predicted molecular weight is 26 kDa and the accession number is A8K660.

Guanylate-binding protein 1 (GBP-1) is a member of the GBP family whose members are GTPases induced in response to interferon-λ (IFN-λ), with seven highly homologous members in humans, termed HuGBP-1 to HuGBP-7. GBP-1 expression is induced by type1 and type2 interferons, including IFN-λ and also by interleukin-1β (IL-1β), IL-1α, and tumor necrosis factor-α (TNF-α). GBP-1 is key to the protective immunity against microbial and viral pathogens. GBP-1 was only secreted from endothelial cells. Secretion occurred without the presence of a leader peptide. Secretion procession is a nonclassical, likely ABC transporter-dependent, pathway and independent of GBP-1 GTPase activity and isoprenylation, and did not require additional interferon-λ-induced factors. Clinically most important was the detection of significantly increased GBP-1 concentrations in the cerebrospinal fluid of patients with bacterial meningitis as compared to control patients.

Adiponectin Protein, Mouse, Recombinant (hFc) is expressed in HEK293 mammalian cells with C-hFc tag. The predicted molecular weight is 51.3 kDa and the accession number is Q60994.

Adiponectin Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 51.6 kDa and the accession number is Q15848.

Atlastin-1, also known as Spastic paraplegia 3 protein A, Guanine nucleotide-binding protein 3, GTP-binding protein 3, GBP3, ATL1 and SPG3A, is a multi-pass membrane protein which belongs to theGBP family and atlastin subfamily. ATL1 / SPG3A is expressed predominantly in the adult and fetal central nervous system. Expression of ATL1 / SPG3A in adult brain is at least 5-fold higher than in other tissues. ATL1 / SPG3A is detected predominantly in pyramidal neurons in the cerebral cortex and the hippocampus of the brain. ATL1 / SPG3A is also expressed in upper and lower motor neurons (at protein level). A distinguishing feature of ATL1 / SPG3A is its frequent early onset, raising the possibility that developmental abnormalities may be involved in its pathogenesis. Missense SPG3A mutant atlastin-1 proteins have impaired GTPase activity and may act in a dominant-negative, loss-of-function manner by forming mixed oligomers with wild-type atlastin-1. Defects in ATL1 / SPG3A are the cause of spastic paraplegia autosomal dominant type 3 (SPG3), also known as Strumpell-Lorrain syndrome. Spastic paraplegia is a degenerative spinal cord disorder characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs.