You Searched For: Palladium+(II)+iodide

Catalog Number: (77528-838)

Supplier: AFG BIOSCIENCE LLC

Description: Human SBDP 150 (Alpha II SPECTRIN BREAKDOWN PRODUCT 150) ELISA Kit

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Supplier: Strem Chemicals Inc

Description: CAS #: 10060-13-6. Size: 500g.

Catalog Number: (77520-444)

Supplier: AFG BIOSCIENCE LLC

Description: Rat CA2 (Carbonic Anhydrase II) ELISA Kit

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Catalog Number: (101418-942)

Supplier: Strem Chemicals Inc

Description: SEGPHOS

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Catalog Number: (RL600-401-873)

Supplier: Rockland Immunochemical

Description: This affinity purified antibody has been tested for use in ELISA and western blot.  Specific conditions for reactivity should be optimized by the end user. Expect a band ~ 54 kDa in size corresponding to CaM Kinase II by western blotting.

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Catalog Number: (10389-134)

Supplier: Bioss

Description: ATG4A is a cysteine protease required for autophagy, which cleaves the C-terminal part of either MAP1LC3, GABARAPL2 or GABARAP, allowing the liberation of form I. A subpopulation of form I is subsequently converted to a smaller form (form II). Form II, with a revealed C-terminal glycine, is considered to be the phosphatidylethanolamine (PE)-conjugated form, and has the capacity for the binding to autophagosomes.

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Catalog Number: (10800-630)

Supplier: Rockland Immunochemical

Description: Coiled-coil domain-containing protein 141 (CCDC141), also known as CAMDI, is a recently identified disrupted in schizophrenia 1 (DISC1)-binding protein that also associates with myosin II. CCDC141 preferentially associates with phosphomyosin II and causes an accumulation of phosphomyosin II at the centrosome in a DISC1-dependent manner. Knockdown of CCDC141 expression by RNAi led to severely impaired radial migration with disoriented chromosomes, suggesting that CCDC141 is required for radial migration through DISC1 and myosin II-mediated centrosome positioning during neuronal development.

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Catalog Number: (10468-330)

Supplier: Bioss

Description: Required during meiosis for separation of sister chromatids and homologous chromosomes. Proteolytic cleavage of REC8 on chromosome arms by separin during anaphase I allows for homologous chromosome separation in meiosis I and cleavage of REC8 on centromeres during anaphase II allows for sister chromatid separation in meiosis II.

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Catalog Number: (77663-590)

Supplier: WORLD PRECISION INSTRUMENTS LLC

Description: Basic kit for anatomy studies.

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Catalog Number: (10072-440)

Supplier: Prosci

Description: The IGFs are mitogenic polypeptide growth factors that stimulate the proliferation and survival of various cell types including muscle, bone, and cartilage tissue in vitro. IGFs are predominantly produced by the liver, although a variety of tissues produce the IGFs at distinctive times. The IGFs belong to the Insulin gene family, which also contains insulin and relaxin. The IGFs are similar by structure and function to insulin, but have a much higher growth-promoting activity than insulin. IGF-II expression is influenced by placenta lactogen, while IGF-I expression is regulated by growth hormone. Both IGF-I and IGF-II signal through the tyrosine kinase type I receptor (IGF-IR), but, IGF-II can also signal through the IGF-II/Mannose-6-phosphate receptor. Mature IGFs are generated by proteolytic processing of inactive precursor proteins, which contain N-terminal and C-terminal propeptide regions. Recombinant murine IGF-I is a 7.6 kDa globular protein containing amino acids including 3 intra-molecular disulfide bonds.

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Catalog Number: (10393-104)

Supplier: Bioss

Description: Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface.

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Catalog Number: (10393-094)

Supplier: Bioss

Description: Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface.

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Catalog Number: (10393-100)

Supplier: Bioss

Description: Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface.

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Catalog Number: (10393-098)

Supplier: Bioss

Description: Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface.

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Catalog Number: (76710-238)

Supplier: AFG BIOSCIENCE LLC

Description: Mouse Casein Kinase II Subunit beta(CSNK2B) ELISA Kit

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Catalog Number: (102114-360)

Supplier: Novus Biologicals

Description: Mouse Monoclonal MHC Class II Polymorphic Antibody (CI.13.I). Tested Applications: Flow Cytometry, Immunohistochemistry, Immunohistochemistry-Frozen. Tested Reactivity: Guinea Pig.

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