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Description:
BMP2 belongs to the transforming growth factor-beta (TGFB) superfamily of secreted growth factors. It is a disulfide-linked homodimer and induces bone and cartilage formation. In addition to its osteogenic activity, BMP2 plays an important role in cardiac morphogenesis and is expressed in a variety of tissues including lung, spleen, brain, liver, prostate ovary and small intestine. The functional form of BMP2 is a 26 kDa protein composed of two identical 114 amino acid polypeptide chains linked by a single disulfide bond. BMPs control fundamental events in early embryonic development, organogenesis and adult tissue homeostasis.
Description:
IQSEC2 is a 1,478 amino acid protein that belongs to the BRAG family and contains one IQ domain, one PH domain and a SEC7 domain. Localizing to the cytoplasm, IQSEC2 is expressed in brain, kidney and small intestine, with weaker levels of expression in placenta, pancreas, ovary, prostate and liver. IQSEC2 is a component of the postsynaptic density at excitatory synapses, and interacts with ARF family members as a guanine nucleotide exchange factor. Through the activation of ARF substrates, IQSEC2 may play a crucial role in cytoskeletal and synaptic organization. The gene encoding IQSEC2 maps to the human X chromosome. Defects to the IQSEC2 gene have been linked to mental retardation X-linked type 1 (MRX1), a condition characterized by decreased intellectual function. IQSEC2 exists as three isoforms due to alternative splicing events.
Description:
Serine/threonine-protein kinase involved in various processes such as cell cycle regulation, gluconeogenesis and lipogenesis regulation, muscle growth and differentiation and tumor suppression. Phosphorylates HDAC4, HDAC5, PPME1, SREBF1, CRTC1/TORC1 and CRTC2/TORC2. Acts as a tumor suppressor and plays a key role in p53/TP53-dependent anoikis, a type of apoptosis triggered by cell detachment: required for phosphorylation of p53/TP53 in response to loss of adhesion and is able to suppress metastasis. Part of a sodium-sensing signaling network, probably by mediating phosphorylation of PPME1: following increases in intracellular sodium, SIK1 is activated by CaMK1 and phosphorylates PPME1 subunit of protein phosphatase 2A (PP2A), leading to dephosphorylation of sodium/potassium-transporting ATPase ATP1A1 and subsequent increase activity of ATP1A1. Acts as a regulator of muscle cells by phosphorylating and inhibiting class II histone deacetylases HDAC4 and HDAC5, leading to promote expression of MEF2 target genes in myocytes. Also required during cardiomyogenesis by regulating the exit of cardiomyoblasts from the cell cycle via down-regulation of CDKN1C/p57Kip2. Acts as a regulator of hepatic gluconeogenesis by phosphorylating and repressing the CREB-specific coactivators CRTC1/TORC1 and CRTC2/TORC2, leading to inhibit CREB activity. Also regulates hepatic lipogenesis by phosphorylating and inhibiting SREBF1. In concert with CRTC1/TORC1, regulates the light-induced entrainment of the circadian clock by attenuating PER1 induction; represses CREB-mediated transcription of PER1 by phosphorylating and deactivating CRTC1/TORC1 (By similarity).
Description:
Core component of multiple SCF-like ECS (Elongin-Cullin 2/5-SOCS-box protein) E3 ubiquitin-protein ligase complexes, which mediate the ubiquitination and subsequent proteasomal degradation of target proteins. As a scaffold protein may contribute to catalysis through positioning of the substrate and the ubiquitin-conjugating enzyme. The functional specificity of the E3 ubiquitin-protein ligase complex depends on the variable substrate recognition component. ECS(SOCS1) seems to direct ubiquitination of JAk2. Seems to be involved poteosomal degradation of p53/TP53 stimulated by adenovirus E1B-55 kDa protein. May form a cell surface vasopressin receptor.
Description:
Proteins internalized into the endocytic pathway are usually degraded. Efficient proteolysis requires denaturation, induced by acidic conditions within lysosomes, and reduction of inter- and intrachain disulfide bonds. Cytosolic reduction is mediated enzymatically by thioredoxin. In the endocytic pathway, reduction of protein disulfide bonds is important for the generation of MHC class II-peptide complexes. This process is catalyzed by a gamma-interferon-inducible thiol reductase (GILT). GILT is synthesized as a precursor, and following delivery to MHC class II-containing compartments (MIICs), is processed to the mature form via cleavage of amino- and carboxy-terminal propeptides. A lysosomal thiol reductase, GILT, is optimally active at low pH and capable of catalyzing disulfide bond reduction both in vivo and in vitro. GILT is expressed constitutively in antigen-presenting cells and is induced by g-interferon in other cell types, suggesting a potentially important role in antigen processing. Additionally, T cell recognition of select exogenous and endogenous epitopes is dependent on tumor cell expression of GILT. The absence of GILT in melanomas alters antigen processing and the hierarchy of immunodominant epitope presentation.
Description:
Aurora A plays a role in cell cycle regulation during anaphase and/or telophase, in relation to the function of the centrosome/spindle pole region during chromosome segregation. Aurora A plays a key role during tumor development and progression and is overexpressed in many human cancers including breast, ovarian and colorectal. Aurora A is viewed as a potential target for anticancer drug treatment.Aurora B is a mitotic protein kinase that phosphorylates histone H3 (probably on Serine 10), behaves as a chromosomal passenger protein, and may regulate several stages of mitosis such as centrosome separation, chromosome segregation and cytokinesis. It localizes to the inner centromere region from prophase to anaphase. The Aurora kinases, members of the Ser/Thr protein kinase family, associate with microtubules during chromosome movement and segregation. Aurora kinase C may play a part in organizing microtubules in relation to the function of the centrosome/spindle pole during mitosis. This protein is localized to centrosome from anaphase to cytokinesis. Expression is limited to testis in normal cells. Elevated expression levels are seen only in a subset of cancer cells such as HepG2, HuH7 and HeLa cells. Aurora-C expression is maximum at M phase.
Description:
Aurora A plays a role in cell cycle regulation during anaphase and/or telophase, in relation to the function of the centrosome/spindle pole region during chromosome segregation. Aurora A plays a key role during tumor development and progression and is overexpressed in many human cancers including breast, ovarian and colorectal. Aurora A is viewed as a potential target for anticancer drug treatment.Aurora B is a mitotic protein kinase that phosphorylates histone H3 (probably on Serine 10), behaves as a chromosomal passenger protein, and may regulate several stages of mitosis such as centrosome separation, chromosome segregation and cytokinesis. It localizes to the inner centromere region from prophase to anaphase. The Aurora kinases, members of the Ser/Thr protein kinase family, associate with microtubules during chromosome movement and segregation. Aurora kinase C may play a part in organizing microtubules in relation to the function of the centrosome/spindle pole during mitosis. This protein is localized to centrosome from anaphase to cytokinesis. Expression is limited to testis in normal cells. Elevated expression levels are seen only in a subset of cancer cells such as HepG2, HuH7 and HeLa cells. Aurora-C expression is maximum at M phase.
Description:
c-Jun NH2-terminal kinases (JNKs) are distant members of the MAP kinase family (1). JNK1 is activated by dual phosphorylation at a Thr-Pro-Tyr motif in response to ultraviolet (UV) light, and it functions to phosphorylate c-Jun at amino terminal serine regulatory sites, Ser-63 and Ser-73, resulting in transcriptional activation (2-5). Two additional JNK family members have been identified as JNK2 and JNK3 (3). JIP-1 (for JNK interacting protein-1) has been identified as a cytoplasmic inhibitor of JNK that retains JNK in the cytoplasm, thereby inhibiting JNK-regulated gene expression. Evidence suggests that JNK1 and JNK2 bind to JIP-1 with greater affinity than to ATF-2 and c-Jun, which are targets of the JNK signaling pathway. JIP-1 contains an amino terminal JNK binding domain and a carboxy terminal SH3 domain. ATF-2 and c-Jun also contain the JNK binding domain and are thought to compete with JIP-1 for JNK binding (6). Multiple splice variants if JIP-1, including JIP-1b, JIP-1c (also designated islet-brain 1 or IB-1), JIP-2a, JIP-2b and JIP-3, have been identified in brain (7).
Description:
RAPGEF6 is a guanine nucleotide exchange factor (GEF) that is expressed in a variety of tissues. Localizing to the cytoplasm and translocated to the plasma membrane upon ligand binding, RAPGEF6 contains an N-terminal Ras-GEF domain, a cyclic nucleotide monophosphate-binding domain, a PDZ (PSD-95/DlgA/ZO-1) domain, a Ras-associating (RA) domain and a Ras exchanger motif. RAPGEF6 is closely related to RAPGEF2 and both proteins exhibit GEF activity specific towards Rap 1 and Rap 2. In addition, RAPGEF6 is capable of binding to M-Ras via its RA domain. Due to alternative splicing events, two additional isoforms exist for RAPGEF6, namely PDZ-GEF2A and PDZ-GEF2B.
Description:
This gene encodes a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. Members of this family share a common protein fold and have diverse functions, such as cell adhesion, cell-cell signalling, glycoprotein turnover, and roles in inflammation and immune response. The encoded protein may play a role in regulating dendritic cell function. Alternative splice variants have been described but their biological nature has not been determined. This gene is closely linked to other CTL/CTLD superfamily members on chromosome 12p13 in the natural killer gene complex region. [provided by RefSeq]
Description:
Defects in SLC2A10 are the cause of arterial tortuosity syndrome (ATS) [MIM:208050]. ATS is an autosomal recessive disorder characterized by tortuosity and elongation of major arteries, often resulting in death at young age. Other typical features include aneurysms of large arteries and stenosis of the pulmonary artery, in association with facial features and several connective tissue manifestations such as soft skin and joint laxity. Histopathological findings include fragmentation of elastic fibers in the tunica media of large arteries.
Description:
Sequence-specific transcription factor which is part of a developmental regulatory system that provides cells with specific positional identities on the anterior-posterior axis.
Description:
Core component of multiple SCF-like ECS (Elongin-Cullin 2/5-SOCS-box protein) E3 ubiquitin-protein ligase complexes, which mediate the ubiquitination and subsequent proteasomal degradation of target proteins. As a scaffold protein may contribute to catalysis through positioning of the substrate and the ubiquitin-conjugating enzyme. The functional specificity of the E3 ubiquitin-protein ligase complex depends on the variable substrate recognition component. ECS(SOCS1) seems to direct ubiquitination of JAk2. Seems to be involved poteosomal degradation of p53/TP53 stimulated by adenovirus E1B-55 kDa protein. May form a cell surface vasopressin receptor.
Description:
Core component of multiple SCF-like ECS (Elongin-Cullin 2/5-SOCS-box protein) E3 ubiquitin-protein ligase complexes, which mediate the ubiquitination and subsequent proteasomal degradation of target proteins. As a scaffold protein may contribute to catalysis through positioning of the substrate and the ubiquitin-conjugating enzyme. The functional specificity of the E3 ubiquitin-protein ligase complex depends on the variable substrate recognition component. ECS(SOCS1) seems to direct ubiquitination of JAk2. Seems to be involved poteosomal degradation of p53/TP53 stimulated by adenovirus E1B-55 kDa protein. May form a cell surface vasopressin receptor.
Description:
Endopeptidase that degrades various components of the extracellular matrix, such as aggrecan and cartilage oligomeric matrix protein (comp), during development, haemostasis and pathological conditions (arthritic disease). May also play a role in neovascularization or angiogenesis. Hydrolyzes collagen type IV, laminin, nidogen, nascin-C isoform, fibronectin, and type I gelatin.
Description:
Sequence-specific transcription factor which is part of a developmental regulatory system that provides cells with specific positional identities on the anterior-posterior axis.
UOM:
1 * 100 µl
Promotion
,BOSSBS-6539R-CY7EA
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