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Protein Page:
LMX1B (human)

Overview
LMX1B Essential for the specification of dorsal limb fate at both the zeugopodal and autopodal levels. Defects in LMX1B are the cause of nail-patella syndrome (NPS); also known as onychoosteodysplasia. NPS is a disease that cause abnormal skeletal patterning and renal dysplasia. 2 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Cell development/differentiation; DNA binding protein; Transcription factor
Cellular Component: nucleus
Molecular Function: protein binding; zinc ion binding; sequence-specific DNA binding; transcription factor activity
Biological Process: cell death; collagen fibril organization; transcription, DNA-dependent; in utero embryonic development; multicellular organismal development; neuron migration; cerebellum morphogenesis; limb morphogenesis; neuron differentiation; organ growth; cell proliferation; regulation of transcription, DNA-dependent; dorsal/ventral pattern formation; midbrain development; positive regulation of transcription from RNA polymerase II promoter; central nervous system neuron development
Reference #:  O60663 (UniProtKB)
Alt. Names/Synonyms: LIM homeobox transcription factor 1, beta; LIM homeobox transcription factor 1-beta; LIM/homeobox protein 1.2; LIM/homeobox protein LMX1B; LMX-1.2; LMX1.2; LMX1B; MGC138325; MGC142051; NPS1
Gene Symbols: LMX1B
Molecular weight: 44,917 Da
Basal Isoelectric point: 6.22  Predict pI for various phosphorylation states
Protein-Specific Antibodies or siRNAs from Cell Signaling Technology® Total Proteins
Select Structure to View Below

LMX1B

Protein Structure Not Found.


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