Mouse Monoclonal Kif 7 antibody [3F8] (STJ96965)

$99.00$319.00

Reactivity: Human, Mouse, Rat
Applications: WB, IF
Conjugation: Unconjugated
Supplier: St John’s Laboratory Ltd.

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Mouse Monoclonal Kif 7 antibody [3F8] (STJ96965)

Supplier: St John’s Laboratory Ltd.

Recommended applications: IHC

Recommended dilution: IHC 1:200

Recommended protocols: check protocols

Image descriptions:

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Alternative names:

Check alternative names for the antibody

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KIF7 antibody, UNQ340/PRO539 antibody,|EQYK340 antibody|kif7 antibody|KIF7_HUMAN antibody|kinesin family member 7 antibody|kinesin like protein KIF7 antibody|Kinesin-like protein kif7 antibody|UNQ340 antibody|Anti-KIF7 antibody (ab95884)
SCBT cat No: sc-107667|

Name

Kif 7 Monoclonal Antibody

Catalogue No.

STJ96965

Reactivity

Human, Mouse, Rat

Specificity

The antibody detects endogenous Kif 7 proteins.

Immunogen

Synthetic Peptide

Host

Mouse

Applications

IHC

Recommended dilution

IHC 1:200

Clonality

Monoclonal

Conjugation

Unconjugated

Isotype

IgG1

Formulation

Kif 7 Antibody was tube-contained. PBS, pH 7.4, containing 0.02% sodium azide as Preservative and 50% Glycerol.

Purification

Kif 7 Antibody was affinity-purified from mouse ascites by affinity-chromatography using specific immunogen.

Storage

-20 Celsius degree. Avoid repeated freeze/thaw cycles.

Alternative antibody names

Kinesin-like protein KIF7 antibody

Database links

Human UniProt/Swiss-Prot:Q2M1P5;Rat UniProt/Swiss-Port: D4A9P0;Human Entrez Gene: 374654;Mouse Entrez Gene: 16576;

Protein names

Kinesin-like protein KIF7

Protein function

Essential for hedgehog signaling regulation: acts as both a negative and positive regulator of sonic hedgehog (Shh) and Indian hedgehog (Ihh) pathways, acting downstream of SMO, through both SUFU-dependent and -independent mechanisms . Involved in the regulation of microtubular dynamics. Required for proper organization of the ciliary tip and control of ciliary localization of SUFU-GLI2 complexes (By similarity). Required for localization of GLI3 to cilia in response to Shh. Negatively regulates Shh signaling by preventing inappropriate activation of the transcriptional activator GLI2 in the absence of ligand. Positively regulates Shh signaling by preventing the processing of the transcription factor GLI3 into its repressor form. In keratinocytes, promotes the dissociation of SUFU-GLI2 complexes, GLI2 nuclear translocation and Shh signaling activation (By similarity). Involved in the regulation of epidermal differentiation and chondrocyte development (By similarity).

Protein tissue specificity

Embryonic stem cells, melanotic melanoma and Jurkat T-cells. Expressed in heart, lung, liver, kidney, testis, retina, placenta, pancreas, colon, small intestin, prostate and thymus.

Involvement in disease

Note: Ciliary dysfunction leads to a broad spectrum of disorders, collectively termed ciliopathies. The ciliopathy range of diseases includes Meckel-Gruber syndrome, Bardet-Biedl syndrome, Joubert syndrome, and hydrolethalus syndrome among others. Single-locus allelism is insufficient to explain the variable penetrance and expressivity of such disorders, leading to the suggestion that variations across multiple sites of the ciliary proteome influence the clinical outcome. Primary ciliopathy loci can be modulated by pathogenic lesions in other ciliary genes to either exacerbate overall severity or induce specific endophenotypes. KIF7 may be causally associated with diverse ciliopathies, and also acts as a modifier gene across the ciliopathy spectrum.; Bardet-Biedl syndrome (BBS) [MIM:209900]: A syndrome characterized by usually severe pigmentary retinopathy, early-onset obesity, polydactyly, hypogenitalism, renal malformation and mental retardation. Secondary features include diabetes mellitus, hypertension and congenital heart disease. Bardet-Biedl syndrome inheritance is autosomal recessive, but three mutated alleles (two at one locus, and a third at a second locus) may be required for clinical manifestation of some forms of the disease. . Note: The gene represented in this entry may act as a disease modifier. Heterozygous missense mutations in KIF7 may genetically interact with other BBS genes and contribute to disease manifestation and severity.; Hydrolethalus syndrome 2 (HLS2) [MIM:614120]: An embryonic lethal disorder characterized by hydrocephaly or anencephaly, postaxial polydactyly of the upper limbs, and pre- or postaxial polydactyly of the lower limbs. Duplication of the hallux is a common finding. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Acrocallosal syndrome (ACLS) [MIM:200990]: A syndrome characterized by hypogenesis or agenesis of the corpus callosum. Clinical features include postaxial polydactyly, hallux duplication, macrocephaly, craniofacial abnormalities, severe developmental delay and mental retardation. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Joubert syndrome 12 (JBTS12) [MIM:200990]: A disorder presenting with cerebellar ataxia, oculomotor apraxia, hypotonia, neonatal breathing abnormalities and psychomotor delay. Neuroradiologically, it is characterized by cerebellar vermian hypoplasia/aplasia, thickened and reoriented superior cerebellar peduncles, and an abnormally large interpeduncular fossa, giving the appearance of a molar tooth on transaxial slices (molar tooth sign). Additional variable features include retinal dystrophy and renal disease. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Pallister-Hall syndrome (PHS) [MIM:146510]: An autosomal dominant disorder characterized by a wide range of clinical manifestations. Clinical features include hypothalamic hamartoma, pituitary dysfunction, central or postaxial polydactyly, and syndactyly. Malformations are frequent in the viscera, e.g. anal atresia, bifid uvula, congenital heart malformations, pulmonary or renal dysplasia. . Note: The gene represented in this entry may be involved in disease pathogenesis.; Al-Gazali-Bakalinova syndrome (AGBK) [MIM:607131]: An autosomal recessive syndrome consisting of macrocephaly, multiple epiphyseal dysplasia and distinctive facial appearance. . Note: The disease is caused by mutations affecting the gene represented in this entry.

Protein sequence and domain

Belongs to the TRAFAC class myosin-kinesin ATPase superfamily. Kinesin family. KIF27 subfamily. / Contains 1 kinesin motor domain.

Protein cellular localization

Cell projection > cilium

Research area

All research areas>Structural Proteins>KIF
(View all antibody categories related to Structural Proteins)

Note

AntibodyPlus can customize Kif 7 Antibody according to your requirement, including bulk product size,etc. Please contact info@antibodyplus.com. AntibodyPlus provide antibody trial sample for your own antibody validation and collects antibody reviews.

Supplier

St John’s Laboratory Ltd.

Product type

Primary antibody

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Immunofluorescence analysis of Mouse colon tissue

1: Kif 7 Monoclonal Antibody(3F8)(red) was diluted at 1:200 (4 degree Celsius,overnight).
2: Cy3 labled Secondary antibody was diluted at 1:300 (room temperature, 50min).
3: Picture B: DAPI(blue) 10min. Picture A:Target. Picture B: DAPI. Picture C: merge of A+B.
 

Immunofluorescence analysis of Mouse colon tissue

1: Kif 7 Monoclonal Antibody(3F8)(red) was diluted at 1:200 (4 degree Celsius,overnight).
2: Cy3 labled Secondary antibody was diluted at 1:300 (room temperature, 50min).
3: Picture B: DAPI(blue) 10min. Picture A:Target. Picture B: DAPI. Picture C: merge of A+B.


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