2824 Results for: "bromfenolová+\u010Derve\u0148"

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: BIOSS INC

PBGD, also designated hydroxymethylbilane synthase, is a cytoplasmic enzyme found in the heme synthesis pathway. PBGD belongs to the HMBS (hydroxymethylbilane synthase) family. Deficiency of PBGD causes errors in pyrrole metabolism, which in turn leads to an inherited autosomal disorder called acute intermittent porphyria (AIP). AIP is characterized by acute attacks of neurological dysfunctions with hypertension, tachycardia, peripheral neurologic disturbances, abdominal pain and excessive amounts of aminolevulinic acid and porphobilinogen in the urine.

Supplier: TONBO BIOSCIENCE

The SN5c antibody is specific for human CD10, a 100 kDa type II transmembrane protein also known as Common Acute Lymphoblastic Leukemia Antigen (CALLA). In normal cells, it is expressed on early B and T lymphoid precursors, neutrophils and on various epithelia. CD10 is also expressed on several lymphoma cells including Burkitt's, acute lymphoblastic, and follicular germinal center lymphomas. CD10 functions as an endopeptidase and is involved in B cell development, as well as a mediator of neutrophil inflammatory responses.

Supplier: BIOSS INC

PBGD, also designated hydroxymethylbilane synthase, is a cytoplasmic enzyme found in the heme synthesis pathway. PBGD belongs to the HMBS (hydroxymethylbilane synthase) family. Deficiency of PBGD causes errors in pyrrole metabolism, which in turn leads to an inherited autosomal disorder called acute intermittent porphyria (AIP). AIP is characterized by acute attacks of neurological dysfunctions with hypertension, tachycardia, peripheral neurologic disturbances, abdominal pain and excessive amounts of aminolevulinic acid and porphobilinogen in the urine.

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: BIOSS INC

PBGD, also designated hydroxymethylbilane synthase, is a cytoplasmic enzyme found in the heme synthesis pathway. PBGD belongs to the HMBS (hydroxymethylbilane synthase) family. Deficiency of PBGD causes errors in pyrrole metabolism, which in turn leads to an inherited autosomal disorder called acute intermittent porphyria (AIP). AIP is characterized by acute attacks of neurological dysfunctions with hypertension, tachycardia, peripheral neurologic disturbances, abdominal pain and excessive amounts of aminolevulinic acid and porphobilinogen in the urine.

Supplier: BIOSS INC

The gene encoding the Mixed-Lineage Leukemia (MLL) proteins is located on chromosome 11q23. Chromosomal translocations involving band 11q23 result in rogue activator proteins that are associated with approximately 10% of patients with acute lymphoblastic leukemia (ALL) and 5% of patients with acute myeloid leukemia (AML). Most patients affected are less than 1 year of age. MLLT11, also known as mixed-lineage leukemia translocated to 11 or AF1q, is a 90 amino acid MLL fusion partner. Based on the expression patterns of MLLT11, it is thought that MLLT11 plays a role in leukemogenesis and, specifically, the progression of acute monocytic leukemia (AML). Also, expressed in embryonic brain cortex, MLLT11 is upregulated during neuronal differentiation and is thought to play a role in the development of the central nervous system. Finally, MLLT11 has been shown to be differentially expressed in highly metastatic cells, in comparison with non-metastatic parent cells. Such findings suggest a role of MLLT11 in tumorigenesis.

Supplier: BIOSS INC

The gene encoding the Mixed-Lineage Leukemia (MLL) proteins is located on chromosome 11q23. Chromosomal translocations involving band 11q23 result in rogue activator proteins that are associated with approximately 10% of patients with acute lymphoblastic leukemia (ALL) and 5% of patients with acute myeloid leukemia (AML). Most patients affected are less than 1 year of age. MLLT11, also known as mixed-lineage leukemia translocated to 11 or AF1q, is a 90 amino acid MLL fusion partner. Based on the expression patterns of MLLT11, it is thought that MLLT11 plays a role in leukemogenesis and, specifically, the progression of acute monocytic leukemia (AML). Also, expressed in embryonic brain cortex, MLLT11 is upregulated during neuronal differentiation and is thought to play a role in the development of the central nervous system. Finally, MLLT11 has been shown to be differentially expressed in highly metastatic cells, in comparison with non-metastatic parent cells. Such findings suggest a role of MLLT11 in tumorigenesis.

Supplier: BIOSS INC

The gene encoding the Mixed-Lineage Leukemia (MLL) proteins is located on chromosome 11q23. Chromosomal translocations involving band 11q23 result in rogue activator proteins that are associated with approximately 10% of patients with acute lymphoblastic leukemia (ALL) and 5% of patients with acute myeloid leukemia (AML). Most patients affected are less than 1 year of age. MLLT11, also known as mixed-lineage leukemia translocated to 11 or AF1q, is a 90 amino acid MLL fusion partner. Based on the expression patterns of MLLT11, it is thought that MLLT11 plays a role in leukemogenesis and, specifically, the progression of acute monocytic leukemia (AML). Also, expressed in embryonic brain cortex, MLLT11 is upregulated during neuronal differentiation and is thought to play a role in the development of the central nervous system. Finally, MLLT11 has been shown to be differentially expressed in highly metastatic cells, in comparison with non-metastatic parent cells. Such findings suggest a role of MLLT11 in tumorigenesis.

Supplier: BIOSS INC

The gene encoding the Mixed-Lineage Leukemia (MLL) proteins is located on chromosome 11q23. Chromosomal translocations involving band 11q23 result in rogue activator proteins that are associated with approximately 10% of patients with acute lymphoblastic leukemia (ALL) and 5% of patients with acute myeloid leukemia (AML). Most patients affected are less than 1 year of age. MLLT11, also known as mixed-lineage leukemia translocated to 11 or AF1q, is a 90 amino acid MLL fusion partner. Based on the expression patterns of MLLT11, it is thought that MLLT11 plays a role in leukemogenesis and, specifically, the progression of acute monocytic leukemia (AML). Also, expressed in embryonic brain cortex, MLLT11 is upregulated during neuronal differentiation and is thought to play a role in the development of the central nervous system. Finally, MLLT11 has been shown to be differentially expressed in highly metastatic cells, in comparison with non-metastatic parent cells. Such findings suggest a role of MLLT11 in tumorigenesis.

Supplier: BIOSS INC

The gene encoding the Mixed-Lineage Leukemia (MLL) proteins is located on chromosome 11q23. Chromosomal translocations involving band 11q23 result in rogue activator proteins that are associated with approximately 10% of patients with acute lymphoblastic leukemia (ALL) and 5% of patients with acute myeloid leukemia (AML). Most patients affected are less than 1 year of age. MLLT11, also known as mixed-lineage leukemia translocated to 11 or AF1q, is a 90 amino acid MLL fusion partner. Based on the expression patterns of MLLT11, it is thought that MLLT11 plays a role in leukemogenesis and, specifically, the progression of acute monocytic leukemia (AML). Also, expressed in embryonic brain cortex, MLLT11 is upregulated during neuronal differentiation and is thought to play a role in the development of the central nervous system. Finally, MLLT11 has been shown to be differentially expressed in highly metastatic cells, in comparison with non-metastatic parent cells. Such findings suggest a role of MLLT11 in tumorigenesis.

Supplier: BIOSS INC

PBGD, also designated hydroxymethylbilane synthase, is a cytoplasmic enzyme found in the heme synthesis pathway. PBGD belongs to the HMBS (hydroxymethylbilane synthase) family. Deficiency of PBGD causes errors in pyrrole metabolism, which in turn leads to an inherited autosomal disorder called acute intermittent porphyria (AIP). AIP is characterized by acute attacks of neurological dysfunctions with hypertension, tachycardia, peripheral neurologic disturbances, abdominal pain and excessive amounts of aminolevulinic acid and porphobilinogen in the urine.

Supplier: BIOSS INC

PBGD, also designated hydroxymethylbilane synthase, is a cytoplasmic enzyme found in the heme synthesis pathway. PBGD belongs to the HMBS (hydroxymethylbilane synthase) family. Deficiency of PBGD causes errors in pyrrole metabolism, which in turn leads to an inherited autosomal disorder called acute intermittent porphyria (AIP). AIP is characterized by acute attacks of neurological dysfunctions with hypertension, tachycardia, peripheral neurologic disturbances, abdominal pain and excessive amounts of aminolevulinic acid and porphobilinogen in the urine.

Supplier: BIOSS INC

The gene encoding the Mixed-Lineage Leukemia (MLL) proteins is located on chromosome 11q23. Chromosomal translocations involving band 11q23 result in rogue activator proteins that are associated with approximately 10% of patients with acute lymphoblastic leukemia (ALL) and 5% of patients with acute myeloid leukemia (AML). Most patients affected are less than 1 year of age. MLLT11, also known as mixed-lineage leukemia translocated to 11 or AF1q, is a 90 amino acid MLL fusion partner. Based on the expression patterns of MLLT11, it is thought that MLLT11 plays a role in leukemogenesis and, specifically, the progression of acute monocytic leukemia (AML). Also, expressed in embryonic brain cortex, MLLT11 is upregulated during neuronal differentiation and is thought to play a role in the development of the central nervous system. Finally, MLLT11 has been shown to be differentially expressed in highly metastatic cells, in comparison with non-metastatic parent cells. Such findings suggest a role of MLLT11 in tumorigenesis.

Supplier: BIOSS INC

Member of GRP1 signaling complexes that are acutely recruited to plasma membrane ruffles in response to insulin receptor signaling. May function as a scaffolding protein.

Supplier: BIOSS INC

Member of GRP1 signaling complexes that are acutely recruited to plasma membrane ruffles in response to insulin receptor signaling. May function as a scaffolding protein.

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: BIOSS INC

PBGD, also designated hydroxymethylbilane synthase, is a cytoplasmic enzyme found in the heme synthesis pathway. PBGD belongs to the HMBS (hydroxymethylbilane synthase) family. Deficiency of PBGD causes errors in pyrrole metabolism, which in turn leads to an inherited autosomal disorder called acute intermittent porphyria (AIP). AIP is characterized by acute attacks of neurological dysfunctions with hypertension, tachycardia, peripheral neurologic disturbances, abdominal pain and excessive amounts of aminolevulinic acid and porphobilinogen in the urine.

Supplier: BIOSS INC

PBGD, also designated hydroxymethylbilane synthase, is a cytoplasmic enzyme found in the heme synthesis pathway. PBGD belongs to the HMBS (hydroxymethylbilane synthase) family. Deficiency of PBGD causes errors in pyrrole metabolism, which in turn leads to an inherited autosomal disorder called acute intermittent porphyria (AIP). AIP is characterised by acute attacks of neurological dysfunctions with hypertension, tachycardia, peripheral neurologic disturbances, abdominal pain and excessive amounts of aminolevulinic acid and porphobilinogen in the urine.

Supplier: BIOSS INC

The Lyl1 gene encodes a basic helix–loop–helix transcription factor involved in T-cell acute lymphoblastic leukemia. The expression of Lyl1 is at higher levels in the majority of cases of acute myeloblastic leukemia (AML) or myelodysplastic syndrome when compared to normal bone marrow. Lyl1 is highly expressed in most AML cell lines.Lyl-1, TAL1 and TAL2 are part of a family of basic helix-loop-helix (bHLH) proteins implicated in T cell acute leukemia. TAL1, also designated SCL, is a serine phosphoprotein and basic helix-loop-helix transcription factor known to regulate embryonic hematopoiesis. TAL2 is a protein involved in T cell acute lymphoblastic leukemia through a chromosomal translocation involving TAL2 and T cell receptor ∫ chain genes. TAL2 includes a helix-loop-helix protein dimerization and DNA-binding domain that is homologous to TAL1 and Lyl-1 proto-oncogenes. Lyl-1 (lymphoblastic leukemia-derived sequence 1) is a nuclear protein. Endogenous Lyl-1 exists in complex with E2å proteins. Lyl-1 and E2å protein can form heterodimeric complexes with distinctive DNA-binding properties in hematolymphoid cells. Lyl-1 is involved in a chromosomal aberration which causes a form of T cell acute lymphoblastic leukemia (T-ALL).