tim1

TIM-1/KIM-1/HAVCR1 Protein, Human, Recombinant (His & hFc) is expressed in HEK293 mammalian cells with hHis and Fc tag. The predicted molecular weight is 57 kDa and the accession number is AAC39862.1.

TIM-1/KIM-1/HAVCR1 Protein, Mouse, Recombinant (His & hFc) is expressed in HEK293 mammalian cells with hHis and Fc tag. The predicted molecular weight is 49 kDa and the accession number is Q3V033.

TIM-1/KIM-1/HAVCR1 Protein, Human, Recombinant (aa 1-135, His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 15.8 kDa and the accession number is AAC39862.1.

Kidney injury molecule 1 (KIM-1, also known as TIM-1) is markedly upregulated in the proximal tubule after injury and is maladaptive when chronically expressed. KIM-1-mediated epithelial cell phagocytosis of apoptotic cells protects the kidney after acute injury by downregulating innate immunity and inflammation. TIM-1/KIM-1/HAVCR1 Protein, Human, Recombinant (aa 21-295, His) is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 30.58 kDa and the accession number is Q96D42.

Kidney injury molecule 1 (KIM-1, also known as TIM-1) is markedly upregulated in the proximal tubule after injury and is maladaptive when chronically expressed. KIM-1-mediated epithelial cell phagocytosis of apoptotic cells protects the kidney after acute injury by downregulating innate immunity and inflammation. TIM-1/KIM-1/HAVCR1 Protein, Cynomolgus, Recombinant (His) is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 35.25 kDa and the accession number is A0A2K5WXJ6.

TIM-1/KIM-1/HAVCR1 Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 31.3 kDa and the accession number is AAC39862.1.

TIM-1/KIM-1/HAVCR belongs to the immunoglobulin superfamily that cosisits 305 amino acid (aa). It is expressed by stimulated T-cells. TIM-1/KIM-1/HAVCR may play a role in T-helper cell development and the regulation of asthma and allergic diseases. Receptor for TIMD4. And may have a role in kidney injury and repair. Belongs to the T-cell and airway phenotype regulator (Tapr) locus, a single chromosomal region that confers reduced T-helper type 2 responsiveness and protects against airway hyperactivity (AHR), the hallmark of human asthma.

TIM-1/KIM-1/HAVCR1 Protein, Canine, Recombinant (mFc) is expressed in HEK293 mammalian cells with mFc tag. The predicted molecular weight is 41.8 kDa and the accession number is A0A8C0N5Y0.

TIM-1/KIM-1/HAVCR1 Protein, Canine, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 17.6 kDa and the accession number is A0A8C0N5Y0.

TIM-1/KIM-1/HAVCR1 Protein, Rat, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 26.7 kDa and the accession number is O54947.

TIM-1/KIM-1/HAVCR1 Protein, Rat, Recombinant (His & hFc) is expressed in HEK293 mammalian cells with hHis and Fc tag. The predicted molecular weight is 52.6 kDa and the accession number is O54947.

TIM-1/KIM-1/HAVCR1 Protein, Rhesus, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 15 kDa and the accession number is BAJ61041.1.

TIM-1/KIM-1/HAVCR1 Protein, Rhesus, Recombinant is expressed in HEK293 mammalian cells. The predicted molecular weight is 32.4 kDa and the accession number is BAJ61041.1.

Mitochondrial import inner membrane translocase subunit TIM14 (TIM14) is an essential component of the PAM complex. PAM complex is required for the translocation of transit peptide-containing proteins from the inner membrane into the mitochondrial matrix in an ATP-dependent manner. In the complex, TIM14 is required to stimulate activity of mtHSP70 (SSC1). TIM14 belongs to the DnaJ family, which has been involved in Hsp40/Hsp70 chaperone systems. As a mitochondrial chaperone, TIM14 functions as part of the TIM23 complex import motor to facilitate the import of nuclear-encoded proteins into the mitochondria. TIM14 also complexes with prohibitin complexes to regulate mitochondrial morphogenesis, and has been implicated in dilated cardiomyopathy with ataxia.

Mitochondrial co-chaperone which forms a complex with prohibitins to regulate cardiolipin remodeling. May be a component of the PAM complex, a complex required for the translocation of transit peptide-containing proteins from the inner membrane into the mitochondrial matrix in an ATP-dependent manner. May act as a co-chaperone that stimulate the ATP-dependent activity.

Mitochondrial import inner membrane translocase subunit TIM16 (TIM16) is an ssential component of the PAM complex. PAM complex is required for the translocation of transit peptide-containing proteins from the inner membrane into the mitochondrial matrix in an ATP-dependent manner. In the complex, TIM16 is required to regulate activity of mtHSP70 (SSC1) via its interaction with PAM18/TIM14. TIM16 may act by positioning PAM18/TIM14 in juxtaposition to mtHSP70 at the translocon to maximize ATPase stimulation.

Stromal interaction molecule 1, also known as STIM1 and GOK, is a cell membrane, a single-pass type I membrane protein and a endoplasmic reticulum membrane protein. STIM1 / GOK is ubiquitously expressed in various human primary cells and tumor cell lines. It contains one EF-hand domain and one SAM (sterile alpha motif) domain. STIM1 / GOK plays a role in mediating Ca2+influx following depletion of intracellular Ca2+stores. It acts as Ca2+sensor in the endoplasmic reticulum via its EF-hand domain. Upon Ca2+depletion, STIM1 / GOK translocates from the endoplasmic reticulum to the plasma membrane where it activates the Ca2+release-activated Ca2+(CRAC) channel subunit, TMEM142A / ORAI1. Transfection of STIM1 / GOK into cells derived from a rhabdoid tumor and from a rhabdomyosarcoma that do not express detectable levels of STIM1 can induce cell death, suggesting a possible role in the control of rhabdomyosarcomas and rhabdoid tumors. Defects in STIM1 are the cause of immune dysfunction with T-cell inactivation due to calcium entry defect type 2 (IDTICED2) which is an immune disorder characterized by recurrent infections, impaired T-cell activation and proliferative response, decreased T-cell production of cytokines, lymphadenopathy, and normal lymphocytes counts and serum immunoglobulin levels.