homologue

Tumor necrosis factor receptor superfamily, member 4 (TNFRSF4), also known as CD134 and OX40 receptor. OX40 is a secondary co-stimulatory immune checkpoint molecule, expressed after 24 to 72 hours following activation; its ligand, OX40L, is also not expressed on resting antigen presenting cells, but is following their activation. OX40/TNFRSF4 Protein (Primary Amine Labeling), Human, Recombinant (hFc), Biotinylated is expressed in HEK293 mammalian cells with C-hFc tag. The predicted molecular weight is 46.8 kDa and the accession number is P43489.

Tumor necrosis factor receptor superfamily, member 4 (TNFRSF4), also known as CD134 and OX40 receptor. OX40 is a secondary co-stimulatory immune checkpoint molecule, expressed after 24 to 72 hours following activation; its ligand, OX40L, is also not expressed on resting antigen presenting cells, but is following their activation. OX40/TNFRSF4 Protein, Human, Recombinant (aa 29-216, His & Avi), Biotinylated is expressed in HEK293 mammalian cells with C-His-Avi tag. The predicted molecular weight is 23.2 kDa and the accession number is P43489.

Tumor necrosis factor receptor superfamily, member 4 (TNFRSF4), also known as CD134 and OX40 receptor. OX40 is a secondary co-stimulatory immune checkpoint molecule, expressed after 24 to 72 hours following activation; its ligand, OX40L, is also not expressed on resting antigen presenting cells, but is following their activation. OX40/TNFRSF4 Protein, Mouse, Recombinant (His & Avi) is expressed in HEK293 mammalian cells with C-His-Avi tag. The predicted molecular weight is 24.2 kDa and the accession number is P47741.

Tumor necrosis factor receptor superfamily, member 4 (TNFRSF4), also known as CD134 and OX40 receptor. OX40 is a secondary co-stimulatory immune checkpoint molecule, expressed after 24 to 72 hours following activation; its ligand, OX40L, is also not expressed on resting antigen presenting cells, but is following their activation. OX40/TNFRSF4 Protein, Human, Recombinant (His & Avi) is expressed in HEK293 mammalian cells with C-His-Avi tag. The predicted molecular weight is 23.2 kDa and the accession number is P43489.

Small ubiquitin-like modifier (SUMO), also known as SUMO homologue and SMT3, is a member of the superfamily of ubiquitin-like polypeptides that become covalently attached to various intracellular target proteins as a way to alter their function, location, and/or half-life. Small ubiquitin-like modifiers include SUMO1, SUMO2, SUMO3, and SUMO4. Except for SUMO4, all other SUMOs are ubiquitously expressed, including in the brain. In human, SUMO2 and SUMO3 are two highly homologous proteins, collectively called SUMO2/3. Several studies suggest that SUMO3 are associated with pathogenesis in several neurological diseases, including Alzheimer's disease, Parkinson's disease, and cerebral ischemia/stroke.

SUMO-Conjugating Enzyme UBC9 (UBC9) belongs to the ubiquitin-conjugating enzyme family. UBC9 is homologous to ubiquitin-conjugating enzymes (E2s). However, instead of conjugating ubiquitin, UBC9 conjugates a ubiquitin homologue, Small Ubiquitin-Like Modifier 1 (SUMO-1). The conjugation of ubiquitin requires the activities of ubiquitin-activating (E1) and conjugating (E2) enzymes. It is suggested that UBC9 might play a role in DNA repair and perhaps even in aging.

The cluster of differentiation (CD) system is commonly used as cell markers in Immunophenotyping. Different kinds of cells in the immune system can be identified through the surface CD molecules associating with the immune function of the cell. There are more than 320 CD unique clusters and subclusters have been identified. Some of the CD molecules serve as receptors or ligands important to the cell through initiating a signal cascade which then alter the behavior of the cell. Some CD proteins do not take part in cell signal process but have other functions such as cell adhesion. CD209b, also known as SIGNR1, is a C-type lectin receptor. CD209b is present on most regions of mouse brain and found on microglia and dendritic cells but not on neurons or astrocytes. CD209b is implicated in the recently described SIGNR1 complement activation pathway, which operates against capsular polysaccharides in splenic marginal macrophages. CD209b in rat is homologue to SIGNR1 in mouse, both of which are found to mediate the uptake of dextran or CPS14 within the splenic marginal zone.

Anterior gradient protein (AGR) 3 is a highly related homologue of pro-oncogenic AGR2 and belongs to the family of protein disulfide isomerases. AGR3 was found in breast, ovary, prostate, and liver cancer, it is associated with the level of differentiation, slowly proliferating tumors, and more favorable prognosis of breast cancer patients. AGR3 is a specialized member of the PDI family that plays an unexpected role in the regulation of CBF and mucociliary clearance in the airway. AGR3 had been characterised as a novel potential biomarker both for breast cancer prognosis and early breast cancer detection from blood.

Ccl12 prevented initiation of the reparative response by prolonging inflammation and inhibiting fibroblast conversion to myofibroblasts, resulting in diminished scar formation. Macrophage secretion of Ccl12 directly impaired fibronectin and collagen deposition and indirectly stimulated collagen degradation through upregulation of matrix metalloproteinase-2. In post-MI patients, circulating LPS levels strongly associated with the Ccl12 homologue monocyte chemotactic protein 1 (MCP-1). Both MCP-1 and MCP-5 are HIF-1 target genes and that HIF-1alpha is involved in transcriptional induction of these two chemokines in astrocytes by hypoxia.

Teneurin-2 is a member of a novel family of transmembrane proteins characterized to date in fish, birds, mammals, and Drosophila (e.g., the pair-rule gene product Ten-m). Teneurin-2, a vertebrate homologue of the Drosophila pair-rule gene ten-m/odz, is revealed to be a membrane-bound transcription regulator. In the nucleus, the intracellular domain of teneurin-2 colocalizes with promyelocytic leukemia (PML) protein in nuclear bodies implicated in transcription control.

Qa-1b binds a peptide (AMAPRTLLL), referred to as Qdm (for Qa-1 determinant modifier), derived from the signal sequence of murine class Ia molecules. This peptide binds with high affinity and accounts for almost all of the peptides associated with this molecule. Human histocompatibility leukocyte antigen (HLA)-E, a homologue of Qa-1b, binds similar peptides derived from human class Ia molecules and interacts with CD94 NKG2 receptors on natural killer cells.

IMPAD1 protein (IMPA3, gPAPP or IMPase 3) belongs to the inositol monophosphatase family. It is found in Purkinje cells, brain stem, lung and chondrocytes. Mouse IMPAD1 gene encodes a type II transmembrane Golgi-embedded glycoprotein with 356 amino acid residues which generates a 306 amino acid residues mature protein after processing. It is expressed in embryo, and in theory may catalyze myo-inositol monophosphate to myo-inositol. Free myo-inositol is used to generate inositol phospholipid, an essential component of intracellular signaling pathways that mobilize calcium. Mouse IMPAD1 exhibits 91% sequence identity with the human homologue.

Ubiquitin-conjugating enzyme E2 A (also known as HHR6A or UBE2A), encoded by human DNA repair genes HHR6A, belongs to the ubiquitin-conjugating enzymes (E2 enzymes) family and is likely to be involved in postreplication repair and induced mutagenesis. UBE2A is described as a CDK2 substrate. It is the human homologue of the product of the Saccharomyces cerevisiae RAD6 / UBC2 gene, a member of the family of ubiquitin-conjugating enzymes. In vivo, HHR6A phosphorylation peaks during the G2/M phase of cell cycle transition, with a concomitant increase in histone H2B ubiquitylation. Mutation of Ser120 to threonine or alanine abolished UBE2A activity, while mutation to aspartate to mimic phosphorylated serine increased UBE2A activity 3-fold. A mutation of UBE2A is considered as the cause of a novel X-linked mental retardation (XLMR) syndrome that affects three males in a two-generation family.