protein

Recombinant Human CLEC4A / CLECSF6 / DCIR Protein (His tag)

MBS2545773

0.02 mg

330 USD

Recombinant Protein

Recombinant Human CLEC4A / CLECSF6 / DCIR Protein (His tag)

[CLEC4A / CLECSF6 / DCIR]

[HDCGC13P, CLECSF6, DCIR, DDB27, LLIR, CLEC4A]

[cochlin isoform b; Cochlin; cochlin; cochlin; COCH-5B2]

[CLEC4A / CLECSF6 / DCIR]

[COCH; COCH; DFNA9; COCH5B2; COCH-5B2; COCH5B2]

Human Cells

> 95 % as determined by SDS-PAGE

Lyophilized from sterile PBS, pH 7.4, 5%trehalose, 5%mannitol, 0.01%Tween80.

Storage: Store it under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted and be used as soon as possible. Avoid repeated freeze-thaw cycles. Stability: Samples are stable for up to twelve months from date of receipt at -70°C

SDS-PAGE

Source: Human. Predicted N terminal: His. Molecular Mass: The recombinant human CLEC4A consists of 184 amino acids and has a calculated molecular mass of 22 kDa. In SDS-PAGE under reducing conditions, rhCLEC4A migrates as an approximately 28 kDa band due to glycosylation. Endotoxin: < 1.0 EU per ug of the protein as determined by the LAL method. Protein Consuntration: A DNA sequence encoding the human CLEC4A (NP_001128530.1) extracellular domain (Gln 70-Leu 237) was expressed, with a polyhistidine tag at the N-terminus

Reconstitution: It is recommended that sterile water (80 ul) be added to the vial to prepare a stock solution of 0.25 mg/mL. Concentration is measured by UV-Vis.

Dendritic cell immunoreceptor (DCIR), also known as C-type lectin domain family 4 member A (CLEC4A), C-type lectin superfamily member 6 (CLECSF6), is a single-pass type II C-type lectin receptor expressed mainly in dendritic cells (DCs), which is a negative regulator of DC expansion and has a crucial role in maintaining the homeostasis of the immune system. The Dectin-2 family of C-type lectins that includes Dectin-2, BDCA-2, DCIR, DCAR, Clecsf8 and Mincle. These type II receptors contain a single extracellular carbohydrate recognition domain and have diverse functions in both immunity and homeostasis. DCIR is the only member of the family which contains a cytoplasmic signalling motif and has been shown to act as an inhibitory receptor, while BDCA-2, Dectin-2, DCAR and Mincle all associate with FcRgamma chain to induce cellular activation, including phagocytosis and cytokine production. Dectin-2 and Mincle have been shown to act as pattern recognition receptors for fungi, while DCIR acts as an attachment factor for HIV. In addition to pathogen recognition, DCIR has been shown to be pivotal in preventing autoimmune disease by controlling dendritic cell proliferation. DCIR expressed on antigen presenting cells and granulocytes and acts as an inhibitory receptor via an intracellular immunoreceptor tyrosine-based inhibitory motif (ITIM). It may also be involved via its ITIM motif in the inhibition of B-cell-receptor-mediated calcium mobilization and protein tyrosine phosphorylation. Additionally, DCIR can participate in the capture of HIV-1 and promote infection in trans and in cis of autologous CD4 (+) T cells from human immature monocyte-derived DCs. DCIR acts as a ligand for HIV-1 and is involved in events leading to productive virus infection. Description: A DNA sequence encoding the human CLEC4A (NP_001128530.1) extracellular domain (Gln 70-Leu 237) was expressed, with a polyhistidine tag at the N-terminus.

205277471

NP_001128530.1

NM_001135058.1

O43405

The protein encoded by this gene is highly conserved in human, mouse, and chicken, showing 94% and 79% amino acid identity of human to mouse and chicken sequences, respectively. Hybridization to this gene was detected in spindle-shaped cells located along nerve fibers between the auditory ganglion and sensory epithelium. These cells accompany neurites at the habenula perforata, the opening through which neurites extend to innervate hair cells. This and the pattern of expression of this gene in chicken inner ear paralleled the histologic findings of acidophilic deposits, consistent with mucopolysaccharide ground substance, in temporal bones from DFNA9 (autosomal dominant nonsyndromic sensorineural deafness 9) patients. Mutations that cause DFNA9 have been reported in this gene. Alternative splicing results in multiple transcript variants encoding the same protein. Additional splice variants encoding distinct isoforms have been described but their biological validities have not been demonstrated. [provided by RefSeq, Oct 2008]

COCH: Plays a role in the control of cell shape and motility in the trabecular meshwork. Defects in COCH are the cause of deafness autosomal dominant type 9 (DFNA9). DFNA9 is a form of sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information. DFNA9 is characterized by onset in the fourth or fifth decade of life and initially involves the high frequencies. Deafness is progressive and usually complete by the sixth decade. In addition to cochlear involvement, DFNA9 patients also exhibit a spectrum of vestibular dysfunctions. Penetrance of the vestibular symptoms is often incomplete, and some patients are minimally affected, whereas others suffer from severe balance disturbances and episodes of vertigo. Affected individuals have mucopolysaccharide depositions in the channels of the cochlear and vestibular nerves. These depositions apparently cause strangulation and degeneration of dendritic fibers. Protein type: Extracellular matrix; Secreted; Secreted, signal peptide. Chromosomal Location of Human Ortholog: 14q12. Cellular Component: extracellular matrix. Molecular Function: collagen binding; protein binding. Biological Process: regulation of cell shape. Disease: Deafness, Autosomal Dominant 9

0.02 mg

330 USD

0.05 mg

635