Full Product Name
PTCH1 Antibody, HRP conjugated
Product Synonym Names
Protein patched homolog 1; PTC; PTC1; PTCH1; PTCH
Product Gene Name
anti-PTCH1 antibody
[Similar Products]
Research Use Only
For Research Use Only. Not for use in diagnostic procedures.
3D Structure
ModBase 3D Structure for Q13635
Purity/Purification
>95%, Protein G purified
Immunogen
Recombinant Human Protein patched homolog 1 protein (1180-1411AA)
Preservative
0.03% Proclin 300
Constituents
50% Glycerol, 0.01M PBS, pH 7.4
Santa Cruz Alternative
Potential replacement for Santa Cruz Biotechnology antibody catalog# sc-6147 / sc-6149 / sc-9016
Preparation and Storage
Shipped at 4 degree C. Upon delivery aliquot and store at -20 degree C or -80 degree C. Avoid repeated freeze.
ISO Certification
Manufactured in an ISO 13485:2003 and EN ISO 13485:2012 Certified Laboratory.
Other Notes
Small volumes of anti-PTCH1 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.
Related Product Information for
anti-PTCH1 antibody
Acts as a receptor for sonic hedgehog (SHH), indian hedgehog (IHH) and desert hedgehog (DHH). Associates with the smoothened protein (SMO) to transduce the hedgehog's proteins signal. Seems to have a tumor suppressor function, as inactivation of this protein is probably a necessary, if not sufficient step for tumorigenesis.
Applications Tested/Suitable for anti-PTCH1 antibody
ELISA (EIA)
NCBI/Uniprot data below describe general gene information for PTCH1. It may not necessarily be applicable to this product.
NCBI Accession #
NP_000255.2
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NCBI GenBank Nucleotide #
NM_000264.3
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UniProt Primary Accession #
Q13635
[Other Products]
UniProt Secondary Accession #
Q13463; Q5R1U7; Q5R1U9; Q5R1V0; Q5VZC0; Q5VZC2; Q86XG7; A3KBI9; E9PEJ8[Other Products]
UniProt Related Accession #
Q13635[Other Products]
Molecular Weight
144,356 Da
NCBI Official Full Name
protein patched homolog 1 isoform L
NCBI Official Synonym Full Names
patched 1
NCBI Official Symbol
PTCH1 [Similar Products]
NCBI Official Synonym Symbols
PTC; BCNS; HPE7; PTC1; PTCH; NBCCS; PTCH11
[Similar Products]
NCBI Protein Information
protein patched homolog 1
UniProt Protein Name
Protein patched homolog 1
UniProt Gene Name
PTCH1 [Similar Products]
UniProt Synonym Gene Names
PTCH; PTC; PTC1 [Similar Products]
UniProt Entry Name
PTC1_HUMAN
NCBI Summary for PTCH1
This gene encodes a member of the patched gene family. The encoded protein is the receptor for sonic hedgehog, a secreted molecule implicated in the formation of embryonic structures and in tumorigenesis, as well as the desert hedgehog and indian hedgehog proteins. This gene functions as a tumor suppressor. Mutations of this gene have been associated with basal cell nevus syndrome, esophageal squamous cell carcinoma, trichoepitheliomas, transitional cell carcinomas of the bladder, as well as holoprosencephaly. Alternative splicing results in multiple transcript variants encoding different isoforms. Additional splice variants have been described, but their full length sequences and
biological validity cannot be determined currently. [provided by RefSeq, Jul 2008]
UniProt Comments for PTCH1
PTCH1: a multi-pass membrane protein member of the ?patched? family that acts as a receptor for sonic hedgehog (SHH), indian hedgehog (IHH) and desert hedgehog (DHH). Associates with the smoothened protein (SMO) to transduce the hedgehog protein?s signal. Seems to have a tumor suppressor function, as inactivation of this protein is probably a necessary, if not sufficient step for tumorigenesis. Interacts with SNX17. Expressed in tumor cells but not in normal skin. In the embryo, found in all major target tissues of sonic hedgehog, such as the ventral neural tube, somites, and tissues surrounding the zone of polarizing activity of the limb bud. Defects in PTCH1 are the cause of basal cell nevus syndrome (BCNS), also known as Gorlin syndrome. BCNS is an autosomal dominant disease characterized by nevoid basal cell carcinomas and developmental abnormalities such as rib and craniofacial alterations, polydactyly, syndactyly, and spina bifida. In addition, the patients suffer from a multitude of tumors like basal cell carcinomas, fibromas of the ovaries and heart, cysts of the skin, jaws and mesentery, as well as medulloblastomas and meningiomas. PTCH1 defects is also the cause of holoprosencephaly, the most common structural anomaly of the brain, in which the developing forebrain fails to correctly separate into right and left hemispheres.
Protein type: Cell cycle regulation; Membrane protein, integral; Membrane protein, multi-pass; Tumor suppressor
Chromosomal Location of Human Ortholog: 9q22.3
Cellular Component: caveola; Golgi apparatus; intracellular membrane-bound organelle; perinuclear region of cytoplasm; plasma membrane
Molecular Function: cholesterol binding; cyclin binding; protein binding; smoothened binding
Biological Process: brain development; dorsal/ventral pattern formation; embryonic limb morphogenesis; limb morphogenesis; negative regulation of multicellular organism growth; negative regulation of osteoblast differentiation; negative regulation of smoothened signaling pathway; negative regulation of transcription factor activity; negative regulation of transcription from RNA polymerase II promoter; neural plate pattern formation; neural tube patterning; organ morphogenesis; pharyngeal system development; protein processing; regulation of smoothened signaling pathway; smoothened signaling pathway
Disease: Basal Cell Carcinoma, Susceptibility To, 1; Basal Cell Nevus Syndrome; Holoprosencephaly 7
Research Articles on PTCH1
1. PTCH1 mutations contribute to as much as 10% of ODA, identify the SHH signaling pathway as a novel effector of SOX2 activity during human ocular development, and indicate that ODA is likely the result of overactive SHH signaling in humans harboring mutations in either PTCH1 or SOX2.
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