TIM 1 Antibody [M14A22] | Primary Antibodies

Application: Reactivity: Mouse

Usage Information

Dilution
WB1:1000 IP1:30 IHC1:2000 IF1:100 FCM1:500

Application
WB, IP, IHC, IF, FCM

Reactivity
Mouse

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
39 kDa 75 kDa,36 kDa, 20-250 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
TIM 1 Antibody [M14A22] detects endogenous levels of total TIM 1 protein.

Clone
M14A22

Synonym(s)
CD365, Kim1, Tim1, Timd1, Havcr1, HAVcr-1, Kidney injury molecule 1, T cell immunoglobulin and mucin domain-containing protein 1, T cell membrane protein 1, T-cell immunoglobulin mucin receptor 1, KIM-1, TIMD-1, TIM-1

Background
TIM‑1 (T‑cell immunoglobulin and mucin domain‑1, HAVCR1) is a type I transmembrane receptor of the TIM family that is expressed on activated CD4⁺ T cells, B cells, invariant NKT cells, and some epithelial cells, where it regulates both adaptive and innate immune responses. The extracellular region contains an Ig‑like domain with a metal‑ion–dependent ligand‑binding site that recognizes phosphatidylserine on apoptotic cell membranes, followed by a heavily glycosylated mucin stalk, while the short cytoplasmic tail carries tyrosine and serine residues that connect TIM‑1 engagement to intracellular signaling cascades. Interaction of TIM‑1 with phosphatidylserine on apoptotic cells or with agonistic antibodies enhances CD4⁺ T‑cell activation, increases expression of Th2‑associated transcription factors, and promotes production of IL‑4, IL‑5, IL‑10, and IL‑13, linking TIM‑1 ligation to skewing of T‑helper differentiation toward Th2 profiles. TIM‑1 expression on T cells is upregulated under Th2‑skewing conditions, that TIM‑1 costimulation augments Th2 cytokine responses and airway eosinophilia, and that genetic or antibody‑mediated interference with TIM‑1 reduces Th2 cytokines and airway inflammation. TIM‑1 is also expressed on invariant NKT cells, where engagement in the presence of TCR stimulation enhances IL‑4 production and reduces IFN‑γ, adding a second route by which TIM‑1 biases effector programs toward type 2 immunity and contributes to airway hyperreactivity after recognition of apoptotic cells.

Background

TIM‑1 (T‑cell immunoglobulin and mucin domain‑1, HAVCR1) is a type I transmembrane receptor of the TIM family that is expressed on activated CD4⁺ T cells, B cells, invariant NKT cells, and some epithelial cells, where it regulates both adaptive and innate immune responses. The extracellular region contains an Ig‑like domain with a metal‑ion–dependent ligand‑binding site that recognizes phosphatidylserine on apoptotic cell membranes, followed by a heavily glycosylated mucin stalk, while the short cytoplasmic tail carries tyrosine and serine residues that connect TIM‑1 engagement to intracellular signaling cascades. Interaction of TIM‑1 with phosphatidylserine on apoptotic cells or with agonistic antibodies enhances CD4⁺ T‑cell activation, increases expression of Th2‑associated transcription factors, and promotes production of IL‑4, IL‑5, IL‑10, and IL‑13, linking TIM‑1 ligation to skewing of T‑helper differentiation toward Th2 profiles. TIM‑1 expression on T cells is upregulated under Th2‑skewing conditions, that TIM‑1 costimulation augments Th2 cytokine responses and airway eosinophilia, and that genetic or antibody‑mediated interference with TIM‑1 reduces Th2 cytokines and airway inflammation. TIM‑1 is also expressed on invariant NKT cells, where engagement in the presence of TCR stimulation enhances IL‑4 production and reduces IFN‑γ, adding a second route by which TIM‑1 biases effector programs toward type 2 immunity and contributes to airway hyperreactivity after recognition of apoptotic cells.

References
https://pubmed.ncbi.nlm.nih.gov/18706830/ https://pubmed.ncbi.nlm.nih.gov/22144095/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%