2824 Results for: "bromfenol´+\u010Derve\u0148"

Supplier: BIOSS INC

Part of the receptor for interleukin 6. Binds to IL6 with low affinity, but does not transduce a signal. Signal activation necessitate an association with IL6ST. Activation may lead to the regulation of the immune response, acute-phase reactions and hematopoiesis.

Supplier: PROSCI

Transcription factor that binds to the interleukin-6 (IL-6)-responsive elements identified in the promoters of various acute-phase protein genes. Activated by IL31 through IL31RA.

Supplier: BIOSS INC

Part of the receptor for interleukin 6. Binds to IL6 with low affinity, but does not transduce a signal. Signal activation necessitate an association with IL6ST. Activation may lead to the regulation of the immune response, acute-phase reactions and hematopoiesis.

Supplier: PROSCI

Transcription factor that binds to the interleukin-6 (IL-6)-responsive elements identified in the promoters of various acute-phase protein genes. Activated by IL31 through IL31RA.

Supplier: PROSCI

Transcription factor that binds to the interleukin-6 (IL-6)-responsive elements identified in the promoters of various acute-phase protein genes. Activated by IL31 through IL31RA.

Supplier: PROSCI

Transcription factor that binds to the interleukin-6 (IL-6)-responsive elements identified in the promoters of various acute-phase protein genes. Activated by IL31 through IL31RA.

Supplier: PROSCI

The tal-1 proto-oncogene encodes a helix-loop-helix DNA-binding protein that has been implicated in the formation of T cell acute lymphoblastic leukemia (T-ALL).

Supplier: ENZO LIFE SCIENCES

Potent and selective leukocyte elastase inhibitor (IC50=44nM). Displays various anti-inflammatory activities including attenuation of LTB4-induced neutrophil migration and serum cytokine levels. Reduces acute inflammatory lung injury in vivo.

Supplier: MP BIOMEDICALS

β-Mercaptoethylamine (Cysteamine hydrochloride) is useful antioxidant. It is experimentally used as a radioprotective agent. It is also used to produce acute and chronic duodenal ulcers in rats and as an antidote to acetaminophen.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.

Supplier: BIOTIUM

This MAb is specific to Complement 4d (C4d) and it reacts with the secreted as well as cell-bound C4d.C4d is a degradation product of the activated complement factor C4b. Complement 4b is typically activated by binding of Abs to specific target molecules. Following activation and degradation of the C4 molecule, thio-ester groups are exposed, which allow transient, covalent binding of the degradation product Complement 4d to endothelial cell surfaces and extracellular matrix components of vascular basement membranes near the sites of C4 activation. The presence of C4d in peritubular capillaries is a key indicator for acute humoral (i.e. antibody-mediated) rejection of kidney, heart, pancreas and lung allografts. As an established marker of antibody-mediated acute renal allograft rejection and its proclivity for endothelium, this component can be detected in peritubular capillaries in chronic renal allograft rejection as well as hyperacute rejection, acute vascular rejection, acute cellular rejection, and borderline rejection. It has been shown to be a significant predictor of transplant kidney graft survival. Anti-C4d, combined with anti-C3d, can be utilized as a tool for diagnosis of allograft rejection that may warrant a prompt and aggressive anti-rejection treatment.