45509 Results for: "L-beta-Homoproline+hydrochloride"

Supplier: Bioss

Fe65L is a 758 amino acid protein that contains one WW domain and two PID domains. Binding to the intracellular domain of the ∫-Amyloid precursor protein, Fe65L is thought to modulate the internalization and, therefore, the accessibility and function of ∫-Amyloid. Via its ability to control the intracellular accumulation of ∫-Amyloid, Fe65L is thought to play a role in the pathogenesis of Alzheimer's disease. Multiple isoforms of Fe65L exist due to alternative splicing events. The gene encoding Fe65L maps to human chromosome 4, which encodes nearly 6% of the human genome and has the largest gene deserts (regions of the genome with no protein encoding genes) of all of the human chromosomes. Defects in some of the genes located on chromosome 4 are associated with Huntington's disease, Ellis-van Creveld syndrome, methylmalonic acidemia and polycystic kidney disease.

Supplier: Bioss

Fe65L is a 758 amino acid protein that contains one WW domain and two PID domains. Binding to the intracellular domain of the ∫-Amyloid precursor protein, Fe65L is thought to modulate the internalization and, therefore, the accessibility and function of ∫-Amyloid. Via its ability to control the intracellular accumulation of ∫-Amyloid, Fe65L is thought to play a role in the pathogenesis of Alzheimer's disease. Multiple isoforms of Fe65L exist due to alternative splicing events. The gene encoding Fe65L maps to human chromosome 4, which encodes nearly 6% of the human genome and has the largest gene deserts (regions of the genome with no protein encoding genes) of all of the human chromosomes. Defects in some of the genes located on chromosome 4 are associated with Huntington's disease, Ellis-van Creveld syndrome, methylmalonic acidemia and polycystic kidney disease.

Supplier: Bioss

Protein Kinase c alpha (PKC alpha) is an 77 kDa member of the conventional group (cPKCs: sensitive to calcium, diacylglycerol, phosphatidylserine and phorbol esters) of the PKC family of serine/ threonine kinases that are involved in a wide range of physiological processes including mitogenesis, cell survival and transcriptional regulation. PKC alpha is an ubiquitously expressed PKC isozyme that has been implicated in the regulation of a broad range of cellular functions including proliferation, differentiation, development, migration, cell cell adhesion, cell extracellular matrix adhesion, and solute transport. The activation loop threonine (threonine 497 in PKC alpha) of conventional PKCs is phosphorylated by phosphoinositide dependent kinase 1 (PDK1). This phosphorylation is necessary for the autophosphorylation of threonine 638 in the carboxy terminus of PKC alpha, a step that is critical for regulating the rate of PKC alpha dephosphorylation and inactivation.

Supplier: Bioss

Apoptosis is a cell death process that removes toxic and/or useless cells during mammalian development. The apoptotic process is accompanied by shrinkage and fragmentation of the cells and nuclei and degradation of the chromosomal DNA into nucleosomal units. DNA fragmentation factor (DFF) is a heterodimeric protein of 40-kD (DFFB) and 45-kD (DFFA) subunits. DFFA is the substrate for caspase-3 and triggers DNA fragmentation during apoptosis. DFF becomes activated when DFFA is cleaved by caspase-3. The cleaved fragments of DFFA dissociate from DFFB, the active component of DFF. DFFB has been found to trigger both DNA fragmentation and chromatin condensation during apoptosis. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene but the biological validity of these variants has not been determined. [provided by RefSeq, Jul 2008].

Supplier: Biotium

β2 microglobulin is a 12 kDa protein with a pI of 5.6. Serum β2 microglobulin levels are a reflection of cell turnover. Levels rise with fever, inflammation, and infection. Increased serum levels are also seen in B-cell malignancies and in renal failure and may indicate a worse prognosis for patients with early-stage Hodgkin's lymphoma. In urine, increased levels are seen in proximal renal tubular disease as well as renal transplant rejection. β2 microglobulin levels can rise either because its rate of synthesis has increased (e.g. in AIDS, malignant monoclonal plasma cell dyscrasia, solid tumours and autoimmune disease) or because of impaired renal filtration (e.g. due to renal insufficiency, graft rejection or nephrotoxicity induced by post-transplantation immunosuppressive therapy).

Supplier: Biotium

β2 microglobulin is a 12 kDa protein with a pI of 5.6. Serum β2 microglobulin levels are a reflection of cell turnover. Levels rise with fever, inflammation, and infection. Increased serum levels are also seen in B-cell malignancies and in renal failure and may indicate a worse prognosis for patients with early-stage Hodgkin's lymphoma. In urine, increased levels are seen in proximal renal tubular disease as well as renal transplant rejection. β2 microglobulin levels can rise either because its rate of synthesis has increased (e.g. in AIDS, malignant monoclonal plasma cell dyscrasia, solid tumours and autoimmune disease) or because of impaired renal filtration (e.g. due to renal insufficiency, graft rejection or nephrotoxicity induced by post-transplantation immunosuppressive therapy).

Supplier: Bioss

Key downstream component of the canonical Wnt signaling pathway. In the absence of Wnt, forms a complex with AXIN1, AXIN2, APC, CSNK1A1 and GSK3B that promotes phosphorylation on N-terminal Ser and Thr residues and ubiquitination of CTNNB1 via BTRC and its subsequent degradation by the proteasome. In the presence of Wnt ligand, CTNNB1 is not ubiquitinated and accumulates in the nucleus, where it acts as a coactivator for transcription factors of the TCF/LEF family, leading to activate Wnt responsive genes. Involved in the regulation of cell adhesion. Acts as a negative regulator of centrosome cohesion. Involved in the CDK2/PTPN6/CTNNB1/CEACAM1 pathway of insulin internalization. Blocks anoikis of malignant kidney and intestinal epithelial cells and promotes their anchorage-independent growth by down-regulating DAPK2. Disrupts PML function and PML-NB formation by inhibiting RANBP2-mediated sumoylation of PML.

Supplier: Bioss

Key downstream component of the canonical Wnt signaling pathway. In the absence of Wnt, forms a complex with AXIN1, AXIN2, APC, CSNK1A1 and GSK3B that promotes phosphorylation on N-terminal Ser and Thr residues and ubiquitination of CTNNB1 via BTRC and its subsequent degradation by the proteasome. In the presence of Wnt ligand, CTNNB1 is not ubiquitinated and accumulates in the nucleus, where it acts as a coactivator for transcription factors of the TCF/LEF family, leading to activate Wnt responsive genes. Involved in the regulation of cell adhesion. Acts as a negative regulator of centrosome cohesion. Involved in the CDK2/PTPN6/CTNNB1/CEACAM1 pathway of insulin internalization. Blocks anoikis of malignant kidney and intestinal epithelial cells and promotes their anchorage-independent growth by down-regulating DAPK2. Disrupts PML function and PML-NB formation by inhibiting RANBP2-mediated sumoylation of PML.

Supplier: Bioss

Apoptosis is a cell death process that removes toxic and/or useless cells during mammalian development. The apoptotic process is accompanied by shrinkage and fragmentation of the cells and nuclei and degradation of the chromosomal DNA into nucleosomal units. DNA fragmentation factor (DFF) is a heterodimeric protein of 40-kD (DFFB) and 45-kD (DFFA) subunits. DFFA is the substrate for caspase-3 and triggers DNA fragmentation during apoptosis. DFF becomes activated when DFFA is cleaved by caspase-3. The cleaved fragments of DFFA dissociate from DFFB, the active component of DFF. DFFB has been found to trigger both DNA fragmentation and chromatin condensation during apoptosis. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene but the biological validity of these variants has not been determined. [provided by RefSeq, Jul 2008].

Supplier: Bioss

Key downstream component of the canonical Wnt signaling pathway. In the absence of Wnt, forms a complex with AXIN1, AXIN2, APC, CSNK1A1 and GSK3B that promotes phosphorylation on N-terminal Ser and Thr residues and ubiquitination of CTNNB1 via BTRC and its subsequent degradation by the proteasome. In the presence of Wnt ligand, CTNNB1 is not ubiquitinated and accumulates in the nucleus, where it acts as a coactivator for transcription factors of the TCF/LEF family, leading to activate Wnt responsive genes. Involved in the regulation of cell adhesion. Acts as a negative regulator of centrosome cohesion. Involved in the CDK2/PTPN6/CTNNB1/CEACAM1 pathway of insulin internalization. Blocks anoikis of malignant kidney and intestinal epithelial cells and promotes their anchorage-independent growth by down-regulating DAPK2. Disrupts PML function and PML-NB formation by inhibiting RANBP2-mediated sumoylation of PML.

Supplier: Abcam

Recombinant Mouse Macrophage Inflammatory Protein 3 alpha is a Full Length protein, in the 28 to 97 aa range, expressed in HEK 293, with ≥95% purity, ≤0,005 EU/µg endotoxin level and suitable for SDS-PAGE, MS, HPLC.

Supplier: Bioss

Fe65L is a 758 amino acid protein that contains one WW domain and two PID domains. Binding to the intracellular domain of the ∫-Amyloid precursor protein, Fe65L is thought to modulate the internalization and, therefore, the accessibility and function of ∫-Amyloid. Via its ability to control the intracellular accumulation of ∫-Amyloid, Fe65L is thought to play a role in the pathogenesis of Alzheimer's disease. Multiple isoforms of Fe65L exist due to alternative splicing events. The gene encoding Fe65L maps to human chromosome 4, which encodes nearly 6% of the human genome and has the largest gene deserts (regions of the genome with no protein encoding genes) of all of the human chromosomes. Defects in some of the genes located on chromosome 4 are associated with Huntington's disease, Ellis-van Creveld syndrome, methylmalonic acidemia and polycystic kidney disease.

Supplier: Bioss

Protein Kinase c alpha (PKC alpha) is an 77 kDa member of the conventional group (cPKCs: sensitive to calcium, diacylglycerol, phosphatidylserine and phorbol esters) of the PKC family of serine/ threonine kinases that are involved in a wide range of physiological processes including mitogenesis, cell survival and transcriptional regulation. PKC alpha is an ubiquitously expressed PKC isozyme that has been implicated in the regulation of a broad range of cellular functions including proliferation, differentiation, development, migration, cell cell adhesion, cell extracellular matrix adhesion, and solute transport. The activation loop threonine (threonine 497 in PKC alpha) of conventional PKCs is phosphorylated by phosphoinositide dependent kinase 1 (PDK1). This phosphorylation is necessary for the autophosphorylation of threonine 638 in the carboxy terminus of PKC alpha, a step that is critical for regulating the rate of PKC alpha dephosphorylation and inactivation.

Supplier: ProSci Inc.

The protein encoded by this gene is part of a complex of proteins that constitute adherens junctions (AJs). AJs are necessary for the creation and maintenance of epithelial cell layers by regulating cell growth and adhesion between cells. The encoded protein also anchors the actin cytoskeleton and may be responsible for transmitting the contact inhibition signal that causes cells to stop dividing once the epithelial sheet is complete. Finally, this protein binds to the product of the APC gene, which is mutated in adenomatous polyposis of the colon. Mutations in this gene are a cause of colorectal cancer (CRC), pilomatrixoma (PTR), medulloblastoma (MDB), and ovarian cancer. [RefSeq].

Supplier: ProSci Inc.

Mutations in nAChRs are found in a rare form of nocturnal frontal lobe epilepsy. Previously, some nAChR mutations have been described that are associated with additional neurological features such as psychiatric disorders or cognitive defects. A new CHRNB2 mutation located in transmembrane region 3 (M3), outside the known ADNFLE mutation cluster. The CHRNB2 mutation I312M, which occurred de novo in twins, markedly increases the receptor's sensitivity to acetylcholine. Phenotypically, the mutation is associated not only with typical ADNFLE, but also with distinct deficits in memory. The cognitive problems are most obvious in tasks requiring the organization and storage of verbal information.

Supplier: ProSci Inc.

This gene is a member of the PAR6 family and encodes a protein with a PSD95/Discs-large/ZO1 (PDZ) domain, an OPR domain and a semi-Cdc42/Rac interactive binding (CRIB) domain. This cytoplasmic protein is involved in asymmetrical cell division and cell polarization processes as a member of a multi-protein complex.This gene is a member of the PAR6 family and encodes a protein with a PSD95/Discs-large/ZO1 (PDZ) domain, an OPR domain and a semi-Cdc42/Rac interactive binding (CRIB) domain. This cytoplasmic protein is involved in asymmetrical cell division and cell polarization processes as a member of a multi-protein complex.

Supplier: ProSci Inc.

alpha Crystallin B Chain (CRYAB) is a cytoplasmic protein that belongs to the small heat shock protein (HSP20) family. Alpha crystallins are composed of two gene products: alpha-A and alpha-B, for acidic and basic, respectively. Alpha crystallins can be induced by heat shock and are members of the small heat shock protein (sHSP also known as the HSP20) family. Alpha crystallins acts as molecular chaperones and hold them in in large soluble aggregates. CRYAB is expressed widely in many tissues and organs. It may contribute to the transparency and refractive index of the lens. The deficiency of CRYAB is the cause of myopathy myofibrillar type 2 (MFM2) and cataract posterior polar type 2 (CTPP2).

Supplier: ProSci Inc.

NDUFB5 is a subunit of the multisubunit NADH:ubiquinone oxidoreductase (complex I). Mammalian complex I is composed of 45 different subunits. It locates at the mitochondrial inner membrane. This protein has NADH dehydrogenase activity and oxidoreductase activity. It transfers electrons from NADH to the respiratory chain. The immediate electron acceptor for the enzyme is believed to be ubiquinone.The protein encoded by this gene is a subunit of the multisubunit NADH:ubiquinone oxidoreductase (complex I). Mammalian complex I is composed of 45 different subunits. It locates at the mitochondrial inner membrane. This protein has NADH dehydrogenase activity and oxidoreductase activity. It transfers electrons from NADH to the respiratory chain. The immediate electron acceptor for the enzyme is believed to be ubiquinone.

Supplier: ProSci Inc.

Thyroid hormones are essential for development of the central nervous system and deficits in these hormones during development affects such cognitive functions as learning and memory (Ambrogini et al., 2005; Chan and Kilby, 2000). Thyroid hormones exert their physiological role mainly through binding to specific nuclear receptors including the predominant isoforms of thyroid hormone receptors TRalpha1, TRalpha2, TRbeta1 and TRbeta2. TRalpha1, TRbeta1 and TRbeta2 bind T3 with high affinity and also bind to thyroid hormone response elements (TREs) on chromatin to regulate the transcriptional processes in several target tissues, including adult rat brain (Constantinou et al., 2005).

Supplier: ProSci Inc.

Cathepsin H (CTSH), which can act both as an aminopeptidase and as an endopeptidase, is a lysosomal cysteine protease of the papain family. CTSH is composed of a dimer of disulfide-linked heavy and light chains, both produced from a single protein precursor. CTSH is associated with various pathological conditions like human fibrous meningioma, colorectal cancer, arthritis, human prostate tumour and lung cancer. CTSH is associated with cancer progression because of their ability to degrade extracellular matrices facilitating invasion, angiogenesis and metastasis as is evident from numerous clinical reports and experimental models. The expression of CTSH is significantly increased in disease states such as in prostate tumours, sera of asthmatic patients, and mucosa of colorectal cancer patients.

Supplier: Antibodies.com

Mouse monoclonal [FYN-01] antibody to FYN for IP, WB, IHC-P and ICC with samples derived from Human and Mouse.

Supplier: Bioss

The protein encoded by this gene is a member of the platelet-derived growth factor family. The four members of this family are mitogenic factors for cells of mesenchymal origin and are characterized by a motif of eight cysteines. This gene product can exist either as a homodimer (PDGF-BB) or as a heterodimer with the platelet-derived growth factor alpha polypeptide (PDGF-AB), where the dimers are connected by disulfide bonds. Mutations in this gene are associated with meningioma. Reciprocal translocations between chromosomes 22 and 7, at sites where this gene and that for COL1A1 are located, are associated with a particular type of skin tumor called dermatofibrosarcoma protuberans resulting from unregulated expression of growth factor. Two alternatively spliced transcript variants encoding different isoforms have been identified for this gene. [provided by RefSeq, Oct 2008].

Supplier: Bioss

Protein Kinase c alpha (PKC alpha) is an 77 kDa member of the conventional group (cPKCs: sensitive to calcium, diacylglycerol, phosphatidylserine and phorbol esters) of the PKC family of serine/ threonine kinases that are involved in a wide range of physiological processes including mitogenesis, cell survival and transcriptional regulation. PKC alpha is an ubiquitously expressed PKC isozyme that has been implicated in the regulation of a broad range of cellular functions including proliferation, differentiation, development, migration, cell cell adhesion, cell extracellular matrix adhesion, and solute transport. The activation loop threonine (threonine 497 in PKC alpha) of conventional PKCs is phosphorylated by phosphoinositide dependent kinase 1 (PDK1). This phosphorylation is necessary for the autophosphorylation of threonine 638 in the carboxy terminus of PKC alpha, a step that is critical for regulating the rate of PKC alpha dephosphorylation and inactivation.

Supplier: Bioss

Apoptosis is a cell death process that removes toxic and/or useless cells during mammalian development. The apoptotic process is accompanied by shrinkage and fragmentation of the cells and nuclei and degradation of the chromosomal DNA into nucleosomal units. DNA fragmentation factor (DFF) is a heterodimeric protein of 40-kD (DFFB) and 45-kD (DFFA) subunits. DFFA is the substrate for caspase-3 and triggers DNA fragmentation during apoptosis. DFF becomes activated when DFFA is cleaved by caspase-3. The cleaved fragments of DFFA dissociate from DFFB, the active component of DFF. DFFB has been found to trigger both DNA fragmentation and chromatin condensation during apoptosis. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene but the biological validity of these variants has not been determined. [provided by RefSeq, Jul 2008].

Supplier: Biotium

β2 microglobulin is a 12 kDa protein with a pI of 5.6. Serum β2 microglobulin levels are a reflection of cell turnover. Levels rise with fever, inflammation, and infection. Increased serum levels are also seen in B-cell malignancies and in renal failure and may indicate a worse prognosis for patients with early-stage Hodgkin's lymphoma. In urine, increased levels are seen in proximal renal tubular disease as well as renal transplant rejection. β2 microglobulin levels can rise either because its rate of synthesis has increased (e.g. in AIDS, malignant monoclonal plasma cell dyscrasia, solid tumours and autoimmune disease) or because of impaired renal filtration (e.g. due to renal insufficiency, graft rejection or nephrotoxicity induced by post-transplantation immunosuppressive therapy).

Supplier: Biotium

β2 microglobulin is a 12 kDa protein with a pI of 5.6. Serum β2 microglobulin levels are a reflection of cell turnover. Levels rise with fever, inflammation, and infection. Increased serum levels are also seen in B-cell malignancies and in renal failure and may indicate a worse prognosis for patients with early-stage Hodgkin's lymphoma. In urine, increased levels are seen in proximal renal tubular disease as well as renal transplant rejection. β2 microglobulin levels can rise either because its rate of synthesis has increased (e.g. in AIDS, malignant monoclonal plasma cell dyscrasia, solid tumours and autoimmune disease) or because of impaired renal filtration (e.g. due to renal insufficiency, graft rejection or nephrotoxicity induced by post-transplantation immunosuppressive therapy).

Supplier: Bioss

Key downstream component of the canonical Wnt signaling pathway. In the absence of Wnt, forms a complex with AXIN1, AXIN2, APC, CSNK1A1 and GSK3B that promotes phosphorylation on N-terminal Ser and Thr residues and ubiquitination of CTNNB1 via BTRC and its subsequent degradation by the proteasome. In the presence of Wnt ligand, CTNNB1 is not ubiquitinated and accumulates in the nucleus, where it acts as a coactivator for transcription factors of the TCF/LEF family, leading to activate Wnt responsive genes. Involved in the regulation of cell adhesion. Acts as a negative regulator of centrosome cohesion. Involved in the CDK2/PTPN6/CTNNB1/CEACAM1 pathway of insulin internalization. Blocks anoikis of malignant kidney and intestinal epithelial cells and promotes their anchorage-independent growth by down-regulating DAPK2. Disrupts PML function and PML-NB formation by inhibiting RANBP2-mediated sumoylation of PML.

Supplier: Bioss

Key downstream component of the canonical Wnt signaling pathway. In the absence of Wnt, forms a complex with AXIN1, AXIN2, APC, CSNK1A1 and GSK3B that promotes phosphorylation on N-terminal Ser and Thr residues and ubiquitination of CTNNB1 via BTRC and its subsequent degradation by the proteasome. In the presence of Wnt ligand, CTNNB1 is not ubiquitinated and accumulates in the nucleus, where it acts as a coactivator for transcription factors of the TCF/LEF family, leading to activate Wnt responsive genes. Involved in the regulation of cell adhesion. Acts as a negative regulator of centrosome cohesion. Involved in the CDK2/PTPN6/CTNNB1/CEACAM1 pathway of insulin internalization. Blocks anoikis of malignant kidney and intestinal epithelial cells and promotes their anchorage-independent growth by down-regulating DAPK2. Disrupts PML function and PML-NB formation by inhibiting RANBP2-mediated sumoylation of PML.

Supplier: Enzo Life Sciences

Autophagy is an alternative process of proteasomal degradation for some long-lived proteins or organelles. Alterations in the autophagic-lysosomal compartment have been linked to neuronal death in many neurodegenerative disorders as well as in transmissible neuronal pathologies (prion diseases). Genetic studies in yeast have shown that Autophagy-defective Gene-8 (Atg-8) represents a specific marker for autophagy. Among the four families of mammalian Atg8-related proteins only LC3 (Microtubule-associated Protein1 Light Chain 3) is expressed at sufficient high levels and efficiently recruited to autophagic vesicles in cells and tissues. During autophagy the cytoplasmic form, LC3-I is processed and recruited to autophagosomes, where LC3-II is generated by site specific proteolysis near to the C-terminus. Autophagic vacuoles have been also reported frequently in cardiomyopathies or muscle cells exposed to different experimental settings.

Supplier: Bioss

Protein Kinase c alpha (PKC alpha) is an 77 kDa member of the conventional group (cPKCs: sensitive to calcium, diacylglycerol, phosphatidylserine and phorbol esters) of the PKC family of serine/ threonine kinases that are involved in a wide range of physiological processes including mitogenesis, cell survival and transcriptional regulation. PKC alpha is an ubiquitously expressed PKC isozyme that has been implicated in the regulation of a broad range of cellular functions including proliferation, differentiation, development, migration, cell cell adhesion, cell extracellular matrix adhesion, and solute transport. The activation loop threonine (threonine 497 in PKC alpha) of conventional PKCs is phosphorylated by phosphoinositide dependent kinase 1 (PDK1). This phosphorylation is necessary for the autophosphorylation of threonine 638 in the carboxy terminus of PKC alpha, a step that is critical for regulating the rate of PKC alpha dephosphorylation and inactivation.